Traditional Chinese medicine composition for treating chronic atrophic gastritis and preparation method thereof

Abstract

The invention belongs to the technical field of traditional Chinese medicines, and particularly relates to a traditional Chinese medicine composition for treating chronic atrophic gastritis and a preparation method of the traditional Chinese medicine composition. Comprising the following raw materials: 2-30 parts of astragalus membranaceus, 2-30 parts of bighead atractylodes rhizome, 1-30 parts of codonopsis pilosula, 1-30 parts of poria cocos, 1-30 parts of Chinese yam, 1-40 parts of salvia miltiorrhiza, 2-30 parts of rhizoma sparganii, 1-40 parts of curcuma zedoary, 1-20 parts of elecampane, 1-20 parts of fructus amomi, 2-30 parts of pericarpium citri reticulatae, 1-30 parts of rhizoma pinellinae praeparata, 1-30 parts of dried ginger, 5-20 parts of coptis chinensis, 1-30 parts of immature bitter orange, 3-30 parts of endothelium corneum gigeriae galli and 2-30 parts of raw liquorice. The traditional Chinese medicine composition disclosed by the invention can be used for effectively treating clinical symptoms of CAG, reversing atrophy, intestinal metaplasia and dysplasia of mucosa, remarkably improving endoscopic manifestation of a CAG patient and promoting lesion of gastric mucosa to be relieved or disappear. Animal experiments show that the traditional Chinese medicine can reduce and reverse lesions such as gastric mucosa gland atrophy and epithelium intestinal metaplasia of CAG rats. Mitochondrial metabolic disorder is a key link of CAG gland atrophy and can effectively block CAG canceration.

Description

Technical Field

[0001] The invention belongs to the technical field of traditional Chinese medicines, and in particular relates to a traditional Chinese medicine composition for treating chronic atrophic gastritis and a preparation method thereof. Background Art

[0002] Atrophic gastritis, also known as chronic atrophic gastritis, is a chronic digestive disease characterized by atrophy of the gastric mucosal epithelium and glands. In this disease, the gastric mucosa becomes thinner and the mucosal base thickens, which may be accompanied by pyloric metaplasia and intestinal metaplasia, or atypical hyperplasia. The disease usually manifests as upper abdominal pain, fullness, belching, loss of appetite, or weight loss, anemia, etc. The causes are diverse, such as Helicobacter pylori infection, eating habits, immune factors, bile or duodenal fluid reflux, etc. Middle-aged and elderly people or those exposed to heavy metals such as lead, mercury, copper and zinc are more susceptible to the disease.

[0003] Symptoms of atrophic gastritis include distension and pain in the epigastric region, heartburn and indigestion, abnormal bowel movements and weakness, anemia, etc. In addition, atrophic gastritis is more likely to be complicated by gastric ulcers, gastric bleeding, anemia, etc. Since the symptoms and signs are non-specific, diagnosis mainly relies on gastroscopy and gastric mucosal biopsy pathology.

[0004] In terms of treatment, in addition to conventional smoking cessation, alcohol abstinence, and dietary adjustment, it is also necessary to give anti-Helicobacter pylori treatment, inhibit bile reflux to improve gastric motility, and give pentagastrin according to the patient's condition. At the same time, increasing mucosal nutrition to enhance the resistance of the gastric mucosa to gastric acid is also part of the treatment.

[0005] According to the latest global cancer data, gastric cancer is still one of the major cancers in the world, with the fifth highest incidence and the fourth highest mortality rate in the world. A large number of studies have shown that chronic atrophic gastritis (CAG) is a chronic digestive system disease in which the gastric mucosal epithelial tissue is damaged for a long time, resulting in a decrease in intrinsic glands, often accompanied by fibrosis replacement, intestinal gland metaplasia / pseudopyloric metaplasia.

[0006] Currently, Western medicines for the treatment of atrophic gastritis mainly include proton pump inhibitors, gastric mucosal protectants, antibiotics and drugs that promote gastric motility, while the proton pump inhibitor rabeprazole is also suitable for atrophic gastritis and has the effect of reducing gastric acid secretion, which may cause adverse reactions such as headache, diarrhea and constipation. Summary of the invention

[0007] In order to solve the above technical problems, an embodiment of the present invention provides a Chinese medicine composition for treating chronic atrophic gastritis.

[0008] To achieve the above object, the embodiments of the present invention adopt the following technical solutions:

[0009] The invention provides a traditional Chinese medicine composition for treating chronic atrophic gastritis. The traditional Chinese medicine composition comprises the following raw materials in parts by weight: 2-30 parts of astragalus, 2-30 parts of atractylodes, 1-30 parts of codonopsis, 1-30 parts of tuckahoe, 1-30 parts of yam, 1-40 parts of salvia, 2-30 parts of trifoliate lancea, 1-40 parts of zedoaria, 1-20 parts of costusroot, 1-20 parts of amomum, 2-30 parts of tangerine peel, 1-30 parts of pinellia, 1-30 parts of dried ginger, 5-20 parts of coptis, 1-30 parts of immature bitter orange, 3-30 parts of chicken's gizzard lining and 2-30 parts of raw liquorice.

[0010] In some embodiments, the Chinese medicine composition for treating chronic atrophic gastritis comprises the following raw materials, by weight: 5-25 parts of Astragalus, 10-30 parts of Atractylodes, 5-25 parts of Codonopsis, 3-28 parts of Poria, 3-26 parts of Dioscorea, 2-35 parts of Salvia, 5-25 parts of Trillium, 2-36 parts of Curcuma, 3-18 parts of Costusroot, 4-18 parts of Amomum, 5-28 parts of Tangerine Peel, 5-25 parts of Pinellia, 3-30 parts of Dry Ginger, 5-18 parts of Coptis, 5-30 parts of Citrus aurantium, 5-30 parts of Chicken Gizzard Stone, and 5-25 parts of Raw Licorice.

[0011] In some embodiments, the Chinese medicine composition for treating chronic atrophic gastritis comprises the following raw materials, by weight: 5-20 parts of Astragalus, 12-28 parts of Atractylodes, 8-25 parts of Codonopsis, 5-25 parts of Poria, 5-24 parts of Dioscorea, 5-30 parts of Salvia, 5-20 parts of Trillium, 3-35 parts of Curcuma, 5-15 parts of Costusroot, 5-15 parts of Amomum, 5-25 parts of Tangerine Peel, 5-20 parts of Pinellia, 4-25 parts of Dry Ginger, 5-15 parts of Coptis, 5-25 parts of Citrus aurantium, 5-20 parts of Chicken Gizzard Stone, and 5-20 parts of Raw Licorice.

[0012] In some embodiments, the Chinese medicine composition for treating chronic atrophic gastritis comprises the following raw materials, by weight: 10-20 parts of Astragalus, 15-20 parts of Atractylodes, 10-20 parts of Codonopsis, 10-25 parts of Poria, 10-20 parts of Dioscorea, 10-20 parts of Salvia miltiorrhiza, 5-15 parts of Trillium, 5-30 parts of Curcuma, 5-10 parts of Costusroot, 5-10 parts of Amomum, 5-20 parts of Citrus reticulata, 5-15 parts of Pinellia, 4-20 parts of dried ginger, 5-10 parts of Coptis chinensis, 5-15 parts of Citrus aurantium, 10-20 parts of Chicken Gizzard Stone, and 5-10 parts of raw licorice.

[0013] In some embodiments, the Chinese medicine composition for treating chronic atrophic gastritis includes the following raw materials, in parts by weight: 20 parts of Astragalus, 15 parts of Atractylodes, 20 parts of Codonopsis, 15 parts of Poria, 15 parts of Dioscorea, 10 parts of Salvia miltiorrhiza, 5 parts of Trillium, 5 parts of Curcuma, 6 parts of Costus root, 6 parts of Amomum villosum, 6 parts of Tangerine peel, 10 parts of Pinellia, 5 parts of Dry Ginger, 5 parts of Coptis chinensis, 6 parts of Citrus aurantium, 15 parts of Chicken Gizzard Stone, and 6 parts of Raw Licorice.

[0014] The present invention also provides a method for preparing a Chinese medicine composition for treating chronic atrophic gastritis, comprising the following steps:

[0015] S1: Weigh astragalus, atractylodes, codonopsis, tuckahoe, yam, salvia, sparganium, curcuma, costusroot, amomum, tangerine peel, pinellia, dried ginger, coptis, immature bitter orange, chicken gizzard lining and raw liquorice according to weight ratio and set aside;

[0016] S2: Mix the Chinese medicinal materials in S1, add 10 to 20 times the weight of the medicinal materials in water, soak for 0.5 to 1 hour, decoct twice, each time for 0.5 to 1 hour, filter the decoction twice, discard the residue, and keep the decoction for later use.

[0017] The Chinese medicine composition of the present invention is composed of astragalus, atractylodes, codonopsis, tuckahoe, yam, salvia, sparganium, curcuma, costus root, amomum, tangerine peel, French pinellia, dried ginger, coptis, immature bitter orange, chicken's gizzard lining, and raw licorice. Among them, astragalus greatly replenishes the qi of the spleen and lungs, makes qi prosperous and blood grows, and protects the skin surface. Atractylodes, codonopsis, tuckahoe, and yam are ministers to help astragalus invigorate the spleen and replenish qi, and restore its transportation and transformation power. Salvia has the characteristics of "removing blood stasis without hurting new blood"; sparganium and curcuma are good at cutting and attacking all accumulations; with amomum and tangerine peel, qi is regulated and stomach is strengthened, French pinellia and dried ginger warm the middle and remove dampness and relieve pain, coptis, immature bitter orange, chicken's gizzard lining detoxify, eliminate accumulation, and guide stagnation, raw licorice clears heat and detoxifies, and the stomach is relieved of poison. The combination of all medicines, attacking and replenishing at the same time, is particularly in line with the core pathogenesis of "spleen deficiency and blood stasis" of CAG.

[0018] Clinical studies have confirmed that the Chinese medicine composition of the present invention can effectively treat the clinical symptoms of CAG, reverse mucosal atrophy, intestinal metaplasia and dysplasia, significantly improve the endoscopic manifestations of CAG patients, and promote the reduction or disappearance of gastric mucosal lesions. Animal experiments show that the Chinese medicine of the present invention can reduce and reverse lesions such as atrophy of gastric mucosal glands and epithelial intestinal metaplasia in CAG rats. Mitochondrial metabolic disorders are the key link in CAG gland atrophy and can effectively block the malignant transformation of CAG. BRIEF DESCRIPTION OF THE DRAWINGS

[0019] Figure 1 This is a comparison of the gastric mucosal efficacy under gastroscopy between the experimental group and the Yiqi Huayu Jiedu prescription group before and after treatment;

[0020] Figure 2 Pathological manifestations of gastric mucosa in the experimental group and the control group (200X);

[0021] Figure 3 This is a gastric function test chart;

[0022] Figure 4 For label free proteomics detection;

[0023] Figure 5 This is the pathological change of rat gastric mucosal epithelial tissue (HE staining, 200X);

[0024] Figure 6 This is the pathological change of rat gastric mucosal epithelial tissue (AB-PAS staining, 200X);

[0025] Figure 7 The ultrastructural changes of rat gastric mucosal epithelium (transmission electron microscope, 8000X);

[0026] Figure 8 For quantitative analysis of ATP in rat gastric mucosal epithelium (luminometer);

[0027] Fig. 9 It is the apoptosis assay of rat gastric mucosal tissue cells (TUNEL, 400X);

[0028] Fig.10 The expression and distribution of PCNA-positive cells in rat gastric mucosal epithelium (IHC, 200X);

[0029] Fig.11 The expression and distribution of KI67 positive cells in rat gastric mucosal epithelium (IHC, 200X);

[0030] Fig.12 for the determination of ROS in rat gastric mucosal epithelium (immunofluorescence, 400X);

[0031] Fig.13 To measure the autophagosome content in rat gastric mucosal tissue (LC3, 400X);

[0032] Fig.14 To detect the level of FOXO3 protein in rat gastric mucosal tissue;

[0033] Fig.15 To measure the FOXO3 protein level in rat gastric mucosal epithelium (IHC, 200X);

[0034] Fig.16 for MC cell viability detection (CCK8);

[0035] Fig.17 To detect the proliferation ability of MC cells (plate clone formation experiment);

[0036] Fig.18 To detect the invasion ability of MC cells (Transwell, 200X);

[0037] Fig.19 For MC cell apoptosis detection;

[0038] Fig. 20 for MC cell cycle differences;

[0039] Fig.21for MC cell mitochondrial damage assay (Mito-Tracker Green, 200X);

[0040] Fig. 22 for MC cell mitochondrial damage assay (JC-1, 200X);

[0041] Fig.23 For MC cell ATP quantitative analysis (luminometer);

[0042] Fig.24 for MC cell ROS assay (DCFH-DA, 400X);

[0043] Fig.25 for MC cell ROS assay (Mito-TrackerRed CMXRos, 200X);

[0044] Fig.26 Detection of FOXO3 protein level in MC cells. DETAILED DESCRIPTION

[0045] The technical solutions in some embodiments of the present disclosure are described clearly and completely below. Obviously, the described embodiments are only part of the embodiments of the present disclosure, not all of the embodiments. Based on the embodiments provided by the present disclosure, all other embodiments obtained by ordinary technicians in this field belong to the scope of protection of the present disclosure.

[0046] Example 1

[0047] S1: Weigh 2g of Astragalus, 2g of Atractylodes, 1g of Codonopsis, 1g of Poria, 1g of Dioscorea, 1g of Salvia, 2g of Tripterygium, 1g of Curcuma, 1g of Aucklandia, 1g of Amomum, 2g of Tangerine Peel, 1g of Pinellia, 1g of Dry Ginger, 5g of Coptis, 1g of Citrus aurantium, 3g of Gallus gallus domesticus and 2g of Raw Licorice, and set aside;

[0048] S2: Mix the Chinese medicinal materials in S1, add 10 times the weight of water to soak for 0.5 hours, decoct twice, each time for 0.5 hours, filter the decoction twice, discard the residue, and keep the decoction for later use.

[0049] Example 2

[0050] S1: Weigh 5g of Astragalus, 5g of Atractylodes, 10g of Codonopsis, 8g of Poria, 6g of Dioscorea, 8g of Salvia, 5g of Tripterygium, 6g of Curcuma, 10g of Aucklandia, 4g of Amomum, 6g of Citrus Reticulata, 6g of Pinellia, 5g of Dry Ginger, 4g of Coptis, 5g of Citrus Aurantium, 3g of Gallus Gallus Ternifolia and 5g of Licorice, and set aside;

[0051] S2: Mix the Chinese medicinal materials in S1, add 12 times the weight of the medicinal materials in water, soak for 0.6 hours, decoct twice, decoct for 0.6 hours each time, filter the decoction twice, discard the residue, and keep the decoction for later use.

[0052] Example 3

[0053] S1: Weigh 15g of Astragalus, 15g of Atractylodes, 15g of Codonopsis, 10g of Poria, 12g of Dioscorea, 13g of Salvia, 8g of Tripterygium, 1-40g of Curcuma, 1-20g of Aucklandia, 1-20g of Amomum, 2-30g of Citrus Reticulata, 1-30g of Pinellia, 1-30g of Dry Ginger, 5-20g of Coptis, 1-30g of Citrus aurantium, 3-30g of Chicken's Gizzard Stone, and 2-30g of Licorice, and set aside;

[0054] S2: Mix the Chinese medicinal materials in S1, add 10 to 20 times the weight of the medicinal materials in water, soak for 0.5 to 1 hour, decoct twice, each time for 0.5 to 1 hour, filter the decoction twice, discard the residue, and keep the decoction for later use.

[0055] Example 4

[0056] S1: Weigh 8g of Astragalus, 6g of Atractylodes, 10g of Codonopsis, 20g of Poria, 15g of Dioscorea, 9g of Salvia, 20g of Tripterygium, 12g of Curcuma, 5g of Aucklandia, 6g of Amomum, 8g of Citrus Reticulata, 12g of Pinellia, 8g of Dry Ginger, 5g of Coptis, 8g of Citrus aurantium, 12g of Gallus gallus domesticus and 5g of Licorice, and set aside;

[0057] S2: Mix the Chinese medicinal materials in S1, add 13 times the weight of the water to soak for 0.6 hours, decoct twice, each time for 0.5 hours, filter the decoction twice, discard the residue, and keep the decoction for later use.

[0058] Example 5

[0059] S1: Weigh 30g of Astragalus, 30g of Atractylodes, 30g of Codonopsis, 30g of Poria, 30g of Dioscorea, 40g of Salvia, 30g of Tripterygium, 40g of Curcuma, 20g of Aucklandia, 20g of Amomum, 30g of Tangerine Peel, 30g of Pinellia, 1-30g of Dry Ginger, 20g of Coptis, 30g of Citrus aurantium, 30g of Chicken Gizzard Stone, and 30g of Raw Licorice, and set aside;

[0060] S2: Mix the Chinese medicinal materials in S1, add 20 times the weight of the water to soak for 1 hour, decoct twice, each time for 1 hour, filter the decoction twice, discard the residue, and keep the decoction for later use.

[0061] Example 6

[0062] S1: Weigh 15g of Astragalus, 20g of Atractylodes, 15g of Codonopsis, 15g of Poria, 10g of Dioscorea, 20g of Salvia, 15g of Tripterygium, 20g of Curcuma, 10g of Aucklandia, 10g of Amomum, 15g of Tangerine Peel, 15g of Pinellia, 15g of Dry Ginger, 10g of Coptis, 15g of Citrus aurantium, 15g of Chicken Gizzard Stone, and 15g of Raw Licorice, and set aside;

[0063] S2: Mix the Chinese medicinal materials in S1, add 15 times the weight of the water to soak for 0.8 hours, decoct twice, each time for 0.8 hours, filter the decoction twice, discard the residue, and keep the decoction for later use.

[0064] Example 7

[0065] S1: Weigh 25g of Astragalus, 28g of Atractylodes, 25g of Codonopsis, 20g of Poria, 25g of Dioscorea, 30g of Salvia, 25g of Tripterygium, 30g of Curcuma, 20g of Aucklandia, 18g of Amomum, 25g of Tangerine Peel, 20g of Pinellia, 25g of Dry Ginger, 15g of Coptis, 25g of Citrus aurantium, 20g of Chicken Gizzard and 25g of Raw Licorice, and set aside;

[0066] S2: Mix the Chinese medicinal materials in S1, add 16 times the weight of the water to soak for 0.8 hours, decoct twice, each time for 0.8 hours, filter the decoction twice, discard the residue, and keep the decoction for later use.

[0067] Example 8

[0068] S1: Weigh 20g of Astragalus, 15g of Atractylodes, 20g of Codonopsis, 15g of Poria, 15g of Dioscorea, 10g of Salvia, 5g of Tripterygium, 5g of Curcuma, 6g of Aucklandia, 6g of Amomum, 6g of Tangerine Peel, 10g of Pinellia, 5g of Dry Ginger, 5g of Coptis, 6g of Citrus aurantium, 15g of Gallus gallus domesticus and 6g of Licorice, and set aside;

[0069] S2: Mix the Chinese medicinal materials in S1, add 10 times the weight of water to soak for 0.5 hours, decoct twice, each time for 0.5 hours, filter the decoction twice, discard the residue, and keep the decoction for later use.

[0070] Example 9

[0071] S1: Weigh 18g of Astragalus, 17g of Atractylodes, 16g of Codonopsis, 20g of Poria, 25g of Dioscorea, 15g of Salvia, 20g of Tripterygium, 16g of Curcuma, 15g of Aucklandia, 12g of Amomum, 20g of Citrus Reticulata, 20g of Pinellia, 15g of Dry Ginger, 10g of Coptis, 20g of Citrus aurantium, 25g of Gallus gallus domesticus and 15g of Licorice, and set aside;

[0072] S2: Mix the Chinese medicinal materials in S1, add 15 times the weight of water to soak for 0.7 hours, decoct twice, each time for 0.7 hours, filter the decoction twice, discard the residue, and keep the decoction for later use.

[0073] Example 10

[0074] S1: Weigh 6g of Astragalus, 8g of Atractylodes, 10g of Codonopsis, 8g of Poria, 10g of Dioscorea, 12g of Salvia, 12g of Tripterygium, 10g of Curcuma, 8g of Aucklandia, 10g of Amomum, 12g of Tangerine Peel, 10g of Pinellia, 8g of Dry Ginger, 15g of Coptis, 10g of Citrus aurantium, 15g of Chicken Gizzard Stone, and 10g of Raw Licorice, and set aside;

[0075] S2: Mix the Chinese medicinal materials in S1, add 14 times the weight of water to soak for 0.8 hours, decoct twice, each time for 0.8 hours, filter the decoction twice, discard the residue, and keep the decoction for later use.

[0076] Embodiment 11

[0077] S1: Weigh 25g of Astragalus, 30g of Atractylodes, 30g of Codonopsis, 25g of Poria, 20g of Dioscorea, 30g of Salvia, 25g of Tripterygium, 20g of Curcuma, 15g of Aucklandia, 10g of Amomum, 25g of Tangerine Peel, 20g of Pinellia, 20g of Dry Ginger, 15g of Coptis, 20g of Citrus aurantium, 20g of Chicken Gizzard, and 20g of Raw Licorice, and set aside;

[0078] S2: Mix the Chinese medicinal materials in S1, add 20 times the weight of the water to soak for 1 hour, decoct twice, each time for 1 hour, filter the decoction twice, discard the residue, and keep the decoction for later use.

[0079] Example 12

[0080] S1: Weigh 15g of Astragalus, 20g of Atractylodes, 10g of Codonopsis, 15g of Poria, 20g of Dioscorea, 15g of Salvia, 20g of Tripterygium, 10g of Curcuma, 8g of Aucklandia, 15g of Amomum, 10g of Citrus Reticulata, 20g of Pinellia, 20g of Dry Ginger, 10g of Coptis, 10g of Citrus Aurantium, 10g of Chicken's Gizzard Stone, and 15g of Raw Licorice, and set aside;

[0081] S2: Mix the Chinese medicinal materials in S1, add 18 times the weight of the medicinal materials in water, soak for 0.5 hours, decoct twice, each time for 1 hour, filter the decoction twice, discard the residue, and keep the decoction for later use.

[0082] Example 13

[0083] S1: Weigh 15g of Astragalus, 14g of Atractylodes, 20g of Codonopsis, 20g of Poria, 15g of Dioscorea, 15g of Salvia, 16g of Tripterygium, 10g of Curcuma, 12g of Aucklandia, 8g of Amomum, 10g of Tangerine Peel, 15g of Pinellia, 10g of Dry Ginger, 15g of Coptis, 18g of Citrus aurantium, 20g of Chicken Gizzard and 10g of Raw Licorice, and set aside;

[0084] S2: Mix the Chinese medicinal materials in S1, add 16 times the weight of the medicinal materials in water, soak for 0.8 hours, decoct twice, decoct for 1 hour each time, filter the decoction twice, discard the residue, and keep the decoction for later use.

[0085] 1. Part I Clinical Trials

[0086] (1) Basis and method for sample size calculation

[0087] According to α=0.05, β=0.2, δ / σ=0.57, the positive drug group (using folic acid tablets, also referred to as the folic acid group) and the Chinese medicine group (using the formula of Example 8, also referred to as the Yiqi Huayu Jiedu prescription group) were arranged in a ratio of 1:1, with 35 cases in each group.

[0088]

[0089] Note: n is the required number of samples, σ is the estimated value of the population standard deviation, and δ is the allowable error.

[0090] (2) Case sources

[0091] All cases were included in the outpatient department and ward of the Department of Spleen and Stomach of Guang'an Traditional Chinese Medicine Hospital. All patients were diagnosed with chronic atrophic gastritis (CAG) by gastroscopy and pathological examination. 70 CAG patients were divided into two groups according to the random number table, 35 cases in the Yiqi Huayu Jiedu prescription group and 35 cases in the folic acid group. The general data (such as age, gender, course of disease, degree of lesions, HP infection) of the two groups were compared without significant differences (P>0.05) and were comparable.

[0092] (3) Diagnostic criteria

[0093] The symptom classification standard refers to the "Guidelines for Clinical Research of New Chinese Medicines" and the "Guidelines for Clinical Research of New Chinese Medicines for the Treatment of Chronic Atrophic Gastritis"; the gastroscopy diagnosis standard refers to the Sydney system (endoscopic part); the pathological diagnosis standard refers to the PavodaGED international grading standard and the classic Jass and other IM grading standards. The HP diagnosis standard refers to the "Fifth National Consensus Report on the Management of Helicobacter pylori Infection" issued by the Gastroenterology Branch of the Chinese Medical Association in Hangzhou, Zhejiang in 2016.

[0094] (4) Inclusion criteria

[0095] Patients diagnosed with chronic atrophic gastritis (spleen and stomach weakness, gastric collateral blood stasis syndrome) by gastroscopy and gastric mucosal biopsy pathological histology (reference diagnostic criteria); aged 18 to 70 years old; confirmed by examination or reexamination within 1 month before the trial; voluntary participation in this trial, and informed consent obtained.

[0096] (5) Exclusion criteria

[0097] Patients with peptic ulcer, gastric space-occupying lesions, or gastric mucosal pathological diagnosis of suspected malignancy; patients with serious primary diseases of the heart, brain, liver, kidney and hematopoietic system, and mental illness; pregnant and lactating women; those with poor compliance, who fail to take medication as prescribed and whose clinical efficacy cannot be determined.

[0098] (6) Exit test criteria

[0099] The subjects experience important organ dysfunction, drug allergic reaction, poor compliance, worsening of the disease or serious adverse reactions during the trial and need to stop the trial drug treatment.

[0100] (7) Criteria for exclusion of cases

[0101] Cases that violated the protocol, such as incorrect treatment grouping, violation of the protocol's combined medication regulations, failure to use medication as prescribed thus affecting the judgment of drug efficacy, incomplete data affecting the judgment of efficacy and safety, and too few cases completed by a single center.

[0102] (8) Treatment methods

[0103] Positive drug group: folic acid tablets, 1 tablet / time, 3 times / day, taken 1 hour before meals. Yiqi Huayu Jiedu prescription group: Example 8 was used. The Chinese medicine decoction machine was made into 150mL / bag by the preparation room of Guang'an Traditional Chinese Medicine Hospital, 1 bag / time, 3 times / day, taken 1 hour before meals. Patients with severe dysplasia were also treated with endoscopic mucosal dissection (ESD).

[0104] (9) Clinical efficacy evaluation

[0105] 1) Clinical manifestation score

[0106] The CAG symptom grading and quantification standard refers to the "Guidelines for Clinical Research of New Chinese Medicines" and uses a table to record the main clinical manifestations of patients: epigastric distension, stomach pain, upper abdominal discomfort, belching, acid reflux, loose stools, fatigue, bitter and dry mouth, nausea and vomiting, noisy stomach, refusal to press painful areas, reduced appetite, chest tightness, constipation, shortness of breath, laziness, vomiting of clear water, bland mouth, yellow urine, dry stools, black stools, and dark complexion. The above clinical manifestations are scored and divided into 4 levels: no (symptoms disappear) is 0 points, mild (patients can be aware of symptoms after being reminded) is 1 point, moderate (patients are aware of symptoms, but it does not affect daily life) is 2 points, and severe (patients are aware of symptoms and it affects daily life) is 3 points. The sum of the scores of various clinical manifestations is the total clinical manifestation score of the patient.

[0107] 2) Gastroscopy

[0108] The procedure was performed once before and after treatment. According to the Sydney system (endoscopic part), the erythema, erosion, atrophy, nodular or granular hyperplasia, and bile reflux of the gastric mucosa were observed under gastroscopy.

[0109] 3) Gastric mucosal pathological examination

[0110] First, 1-2 pieces of gastric mucosal tissue were taken from the lesion, and another piece was routinely taken from the gastric angle, 1 piece was taken from the lesser curvature and greater curvature 2 cm away from the pyloric orifice, and 1 piece was taken from the greater curvature and lesser curvature 8 cm away from the cardia. The gastric mucosal tissue blocks were used for pathological HE staining and for morphological analysis of gastric mucosal pathological tissue. The pathological histological scoring standard was based on the "Guidelines for Clinical Research of New Chinese Medicines".

[0111] 4) Helicobacter pylori (HP) assay

[0112] HP infection was determined by C14 breath test, once before and after treatment. HP diagnostic criteria refer to the "Fifth National Consensus Report on the Management of Helicobacter pylori Infection" issued by the Gastroenterology Branch of the Chinese Medical Association in Hangzhou, Zhejiang in 2016.

[0113] 5) Detect the levels of serum pepsinogen I, pepsinogen II, and gastrointestinal hormones (gastrin GAS, motilin MTL, and prostacyclin E2) in patients.

[0114] 6) Safety evaluation

[0115] The three major routine tests, liver and kidney function tests, and electrocardiogram routine tests are performed once before and after treatment.

[0116] (10) Statistical analysis

[0117] SPSS17.0 statistical software was used for processing. Enumeration data were expressed as frequency (f), sample composition ratio was expressed as mean rank (R), and the Mann-Whitney test was used for pairwise comparison of mean rank between groups. Measurement data were expressed as mean plus or minus standard deviation (x±s), paired sample t test was used for intra-group comparison, and independent sample t test was used for inter-group comparison. α=0.05.

[0118] (11) Results

[0119] The specific research results are as follows:

[0120] 1) Recruit CAG patients, the general information of the patients is as follows

[0121] 70 CAG patients were recruited and divided into the Yiqi Huayu Jiedu prescription group (experimental group) with 35 patients and the folic acid group (control group) with 35 patients. There was no significant difference in the basic information of the two groups, such as gender, age, and course of disease. See Table 1.

[0122] Table 1 Comparison of general conditions between the experimental group and the control group

[0123] Group n Gender (male / female) Age / years Disease duration / year Experimental Group 35 20 / 15 47.54±9.68 9.17±6.33 Control group 35 22 / 13 46.76±9.36 8.92±6.56

[0124] 2) Cases included in the analysis

[0125] In the actual trial, 5 patients in the trial group could not take the medicine on time and withdrew from the trial. 4 patients in the control group could not take the medicine on time and withdrew from the trial, and 1 patient took other drugs on his own and withdrew from the trial. Therefore, a total of 60 cases were included in the analysis, 30 in the trial group and 30 in the control group. Comparison of the pathological degree between the two groups showed that in the trial group, there were 5 cases of mild mucosal atrophy, 17 cases of moderate mucosal atrophy, and 8 cases of severe mucosal atrophy; 7 cases of mild intestinal metaplasia, 12 cases of moderate mucosal atrophy, and 3 cases of severe mucosal atrophy; 13 cases of mild dysplasia, 6 cases of moderate mucosal atrophy, and 1 case of severe mucosal atrophy. In the control group, there were 7 cases of mild mucosal atrophy, 16 cases of moderate mucosal atrophy, and 7 cases of severe mucosal atrophy; 9 cases of mild intestinal metaplasia, 12 cases of moderate mucosal atrophy, and 2 cases of severe mucosal atrophy; 12 cases of mild dysplasia, 6 cases of moderate mucosal atrophy, and 1 case of severe mucosal atrophy.

[0126] 3) Clinical manifestation score

[0127] There was no statistical difference in the TCM symptom scores of the two groups of patients before treatment, and they were comparable. After treatment, the TCM symptom scores of both the experimental group and the control group decreased significantly compared with those before treatment, and the differences were statistically significant. Compared with the TCM symptom scores of the two groups after treatment, the TCM symptom scores of the experimental group decreased more significantly, and the difference was statistically significant. See Table 2. The above results show that the Yiqi Huayu Jiedu prescription group can significantly improve the clinical symptoms of CAG patients.

[0128] Table 2 Comparison of TCM symptom scores

[0129]

[0130]

[0131] 4) Gastroscopy

[0132] There was no statistical difference in the endoscopic lesion scores of the two groups of patients before treatment, and they were comparable. After treatment, there were 1 case of severe gastric mucosal lesions under gastroscopy in the experimental group, 6 cases of moderate gastric mucosal lesions, 20 cases of mild gastric mucosal lesions, and 3 cases of no lesions, while there were 1 case of severe gastric mucosal lesions, 13 cases of moderate gastric mucosal lesions, 16 cases of mild gastric mucosal lesions, and 0 cases of no lesions in the control group. The endoscopic scores of both groups were significantly decreased compared with those before treatment, and the differences were statistically significant. Comparing the endoscopic scores of the two groups after treatment, the endoscopic scores of the experimental group decreased more significantly, but there was no significant statistical significance. See Table 3 and Figure 1 The above results showed that the Yiqi Huayu Jiedu prescription group could improve the signs of gastric mucosal lesions under gastroscopy in patients with CAG.

[0133] Table 3 Comparison of gastroscopy efficacy

[0134]

[0135] 5) Gastric mucosal pathological examination

[0136] There was no statistical difference in the gastric mucosal pathology scores of the two groups of patients before treatment, and they were comparable. After treatment, the gastric mucosal pathology scores of both the experimental group and the control group decreased significantly compared with those before treatment, and the differences were statistically significant. Compared with the pathology scores of the two groups after treatment, the pathology scores of the experimental group decreased more significantly, and the difference was statistically significant. See Table 4 and Figure 2 The above results showed that the Yiqi Huayu Jiedu prescription group could significantly improve abnormal pathological changes such as gastric mucosal atrophy and intestinal metaplasia in patients with CAG.

[0137] Table 4 Comparison of pathological efficacy

[0138] Grouping Number of cases Before treatment After treatment Experimental Group 30 12.52±5.10 6.48±4.12 Control group 30 12.21±4.89 9.03±4.27

[0139] 6) Hp determination

[0140] There was no statistical difference in the pathological scores of the two groups of patients before treatment, and they were comparable. After treatment, the HP infection rates of the experimental group and the control group decreased slightly compared with those before treatment, but the differences were not statistically significant. See Table 5. The above results show that the Yiqi Huayu Jiedu prescription has no significant intervention effect on HP infection in CAG patients.

[0141] Table 5 Comparison of HP infection

[0142] Grouping Number of cases Before treatment After treatment Experimental Group 30 17(+)13(-) 12(+)18(-) Control group 30 15(+)15(-) 13(+)17(-)

[0143] 7) Detect the levels of serum pepsinogen I (PGI), pepsinogen II (PGII), and gastrointestinal hormones (gastrin GAS, motilin MTL, and prostacyclin E2) in patients.

[0144] After treatment, the gastric function of both the experimental group and the control group changed significantly compared with that before treatment, and the differences were statistically significant. Comparing the PGII, GAS, and MTL indicators of the two groups after treatment, the gastric function score of the experimental group decreased more significantly, and the difference was statistically significant. Comparing the PGI and PGE2 indicators of the two groups after treatment, the gastric function of the experimental group increased more significantly, and the difference was statistically significant. Figure 3 The above results show that the Yiqi Huayu Jiedu recipe can significantly improve the abnormal changes in gastric function in CAG patients.

[0145] 8) Safety evaluation

[0146] There were no abnormal changes in the patient's three routine tests, liver and kidney function, and electrocardiogram routine tests before and after treatment.

[0147] 2. Part II Clinical Trials

[0148] (1) Basis and method for sample size calculation

[0149] According to α=0.05, β=0.2, δ / σ=0.57, the normal control group and the Chinese medicine group (Yiqi Huayu Jiedu prescription group) were arranged in a 1:1 ratio, with 35 cases in each group.

[0150]

[0151] Note: n is the required number of samples, σ is the estimated value of the population standard deviation, and δ is the allowable error.

[0152] (2) Case sources

[0153] All cases were included in the outpatient department and ward of the Department of Spleen and Stomach of Guang'an Traditional Chinese Medicine Hospital. All patients were diagnosed with chronic atrophic gastritis (CAG) by gastroscopy and pathological examination. 35 CAG patients were in the Yiqi Huayu Jiedu prescription group. 35 healthy volunteers were recruited as the normal control group. It was ensured that there was no significant difference in the general data (such as age and gender) between the two groups and that they were comparable.

[0154] (3) Diagnostic criteria, (4) Inclusion criteria, (5) Exclusion criteria, (6) Withdrawal criteria, and (7) Case exclusion criteria.

[0155] The above five standards are the same as those in the first part of clinical trials and will not be repeated here.

[0156] (8) Treatment methods

[0157] Yiqi Huayu Jiedu prescription group (CAG medication group): Example 8 was used. The Chinese medicine decoction machine was used in the preparation room of Guang'an Traditional Chinese Medicine Hospital to prepare 150 mL / bag, 1 bag / time, 3 times / day, and taken 1 hour before meals. Patients with severe dysplasia were treated with endoscopic mucosal dissection (ESD) at the same time.

[0158] (9) Sample measurement

[0159] The samples were divided into a normal group, a group before CAG administration, and a group after CAG administration. There were 6 samples in each group, and the gastric mucosa was tested by label-free proteomics. Figure 4 As shown, compared with the control group, there was a significant difference in the protein expression of the CAG medication group, suggesting that the Yiqi Huayu Jiedu recipe can effectively change the protein expression in the gastric mucosa of CAG lesions to treat CAG.

[0160] 3. Animal experiments

[0161] (1) Construction of CAG rat model

[0162] Forty SPF SD rats, half male and half female, aged 4-6 weeks, weighing 120-150 g, were randomly divided into a blank group (10 rats) and a modeling group (30 rats). The blank group rats had a normal diet, and the modeling group rats were constructed with the classic MNNG-ammonia compound modeling method to construct the CAG rat model.

[0163] (2) Preparation of Chinese medicine

[0164] Yiqi Huayu Jiedu prescription (YQHY) group: Example 8 was used. The decoction was prepared by the Chinese Medicine Preparation Center of the Affiliated Hospital of Chengdu University of Traditional Chinese Medicine, and the drug was concentrated to 3 g / mL and stored in a 4°C refrigerator for later use.

[0165] (3) Identification of CAG rat model

[0166] At 6 weeks after modeling, 2 rats were randomly selected from the modeling group and the CAG lesions in the gastric mucosa were detected by HE staining.

[0167] (4) Grouping and dosing method

[0168] Except for 10 rats in the normal feeding blank control group, the rest of the model rats were randomly divided into: model control group, YQHY-L group, and YQHY-H group, with 10 rats in each group. Starting from the 6th week, rats in each group began to be gavaged for 12 consecutive weeks, as follows: ① Blank control group and model control group: distilled water 1mL / 100g / time / d gavage; ② YQHY-L group: 15.3g / kg / time / d (equivalent to adult clinical equivalent) gavage; ③ YQHY-H group: 30.6g / kg / time / d (2 times adult clinical equivalent) gavage.

[0169] (5) Preparation of gastric mucosal tissue specimens

[0170] After the 18th week, tissues from the lesion were taken and paraffin sections were made. The remaining gastric mucosal tissues were immediately stored in a -80℃ low-temperature refrigerator.

[0171] (6) Index measurement and analysis

[0172] 1) First, we performed HE staining on the animal tissue. HE staining, the full name of which is hematoxylin-eosin staining, is a staining technique that is extremely commonly used in the fields of histology and pathology. Its main purpose is to clearly observe the morphological structure of cells and tissues under a microscope. First, we fixed the tissue samples in a 10% neutral formalin solution for 8 hours to ensure that the proteins and other cellular components in the tissue are fully cross-linked, thereby preserving the original structure and morphology of the tissue. Subsequently, the fixed tissue samples were dehydrated. This step was completed through a series of ethanol solutions with gradually increasing concentrations (70%, 80%, 90%, 95% and 100%) to ensure that ethanol can gradually replace the water in the tissue until the tissue is completely dehydrated. The dehydrated tissue was then transparentized, that is, the tissue was immersed in xylene. The role of xylene is to replace the ethanol in the tissue and make the tissue transparent, so that paraffin can better penetrate into the tissue, laying the foundation for the subsequent wax dipping step. The transparent tissue was immersed in molten paraffin, and the paraffin was changed three times during the period to ensure that the tissue was completely soaked in paraffin. The wax-impregnated tissue is then embedded in paraffin to form a block that can be sliced. Next, a microtome is used to cut the paraffin block into slices with a thickness of 4-8 microns and attach them to a slide, ready for dewaxing and hydration. The paraffin on the slices is then removed through a series of different concentrations of ethanol and xylene treatments, making the slices moist again for easy staining. Hydration is to soak the dewaxed slices in distilled water to allow them to reabsorb water. Next is staining. First, the slices are placed in hematoxylin stain for 10 minutes. The acidic substances in the cell nucleus combine with hematoxylin to appear blue. After staining, the slices are rinsed with tap water to remove excess stain. Then, the slices are placed in 1% hydrochloric acid alcohol for differentiation to remove non-specific staining until the blue color of the cell nucleus is clearly visible and the background is colorless. After differentiation is complete, wash again. Next, the blueing is performed by placing the slices in lithium carbonate solution. This process can neutralize the hydrochloric acid and make the blue color of the cell nucleus brighter and easier to observe. Subsequently, the sections are placed in eosin stain for 3 minutes, and the alkaline substances in the cytoplasm combine with eosin and stain red. After staining, the sections are dehydrated through a series of different concentrations of ethanol and placed in xylene again for transparency. Finally, the sections are sealed with a mounting medium such as neutral gum or Canada balsam and covered with a coverslip to protect the sections and facilitate long-term storage. At this point, the HE-stained sections can be observed and analyzed under an optical microscope, and the blue color of the cell nucleus contrasts sharply with the red color of the cytoplasm.

[0173] HE staining showed that the glandular structure of gastric mucosal tissue in the normal group was intact and the boundaries were clear. The gastric pits, single-layer columnar epithelium, and lamina propria were well preserved under the light microscope, and their positions and proportions remained unchanged. The nuclei of gastric mucosal epithelial cells were oval, the cytoplasm was lightly stained, the nuclear polarity was intact, and nuclear division was occasionally seen. In the model group, the epithelium of gastric mucosal tissue of rats showed dysplastic changes, which were manifested as obvious disorder and crowding of the glandular structure in the gastric mucosal epithelial tissue, unclear boundaries of the glandular cavity, and "back-to-back" or stratified changes; the gastric mucosal epithelial cells were of different sizes and had obvious atypia. The nuclei were deeply stained, enlarged, overlapped, and the polarity was significantly weakened. The nucleoli were prominent, and obvious nuclear division was seen on the basal side. In the rats in the Chinese medicine intervention group, the gastric mucosal epithelium was mostly benign reactive hyperplasia, and low-grade dysplasia was occasionally seen. In particular, the arrangement of glandular ducts and back-to-back tubular structures were significantly improved compared with the model group. The glandular structure in the gastric mucosal epithelial tissue is slightly or moderately disordered, the border of the glandular cavity is unclear, and there is rarely a "back-to-back" or stratified change; the gastric mucosal epithelial cells show moderate atypical changes, with different sizes, dark staining, enlargement, overlap, and weakened polarity of the nucleus, prominent nucleoli, and obvious nuclear division on the basal side ( Figure 5 ). This result indicates that YQHY intervention can improve the pathological changes of gastric mucosa in CAG rats and treat CAG.

[0174] 2) We further evaluated the severity of chronic atrophic gastritis (CAG) in rats by performing AB-PAS staining. AB-PAS staining is a histochemical staining technique that combines Alcian blue (AB) and periodic acid-Schiff (PAS) reaction to detect acidic mucopolysaccharides and carbohydrates in tissues. First, tissue samples were fixed, dehydrated, cleared, and waxed, then cut into thin sections and attached to slides. Next, the sections were dewaxed in xylene and hydrated through an ethanol series, followed by oxidation in a 0.5% periodic acid solution to expose carbohydrates, and excess periodic acid was washed with water. After that, the sections were incubated in Schiff's reagent to allow the oxidized carbohydrates to react with fuchsin to form a red precipitate, and then washed again. Next, the sections were stained in a 1% Alcian blue solution to make the acidic mucopolysaccharides appear blue, then washed with water and differentiated if necessary. Finally, the sections were dehydrated through ethanol, cleared in xylene, and mounted with neutral gum or Canada balsam. Under a microscope, acidic mucopolysaccharides appear blue or green, while carbohydrates appear red, which can simultaneously display the presence and distribution of these two components. This staining method is particularly important in pathological diagnosis. During AB-PAS staining, acidic mucins in gastric mucosal epithelial cells are specifically labeled in blue, while neutral mucins are labeled in red.

[0175] Under an optical microscope, we carefully observed the gastric mucosal tissue of CAG rats. The results showed that a large number of blue or purple plaques appeared on the gastric mucosa of these rats. The formation of these plaques indicated that the intestinal mucosa had undergone significant pathological changes, and the content of acidic mucin increased significantly, thus revealing the severity of CAG. At the same time, we compared and observed the rats treated with the YQHY treatment regimen. On the gastric mucosa of these rats, the appearance of blue or purple plaques was significantly reduced, and the color was lightened ( Figure 6 ). This result shows that YQHY treatment alleviated the pathological changes of CAG rats to a great extent and effectively reduced the content of acidic mucin, thereby improving the symptoms of chronic atrophic gastritis. It can be seen that the YQHY treatment regimen has a significant effect in the treatment of CAG and provides a useful reference for clinical treatment.

[0176] 3) Transmission electron microscopy observation of mitochondria begins with sample preparation. Fresh rat gastric epithelial tissue is selected and cut into blocks with a side length of 3 mm. Then, it is double-fixed with glutaraldehyde and osmium acid to maintain the integrity of the cell structure. The fixed samples undergo a series of dehydration treatments, using ethanol and acetone to gradually replace the water in the cells. Subsequently, the samples are infiltrated in a low-viscosity resin and embedded in pure resin, which is polymerized to form a hard block for ultrathin sectioning. An ultrathin slicer is used to cut the embedded blocks into 50-70 nanometer thick slices, which are fished out onto a copper grid covered with Formvar. Next, the slices are stained in uranyl acetate and lead citrate to enhance the contrast under the electron microscope.

[0177] The stained sections were observed under a transmission electron microscope. The electron beam penetrated the ultrathin sections to record the microstructure of the mitochondria, including the double membrane structure, the arrangement of cristae, the matrix content, and possible damage or variant morphology. Compared with the control group, the mitochondria in the gastric mucosa of the rats in the model group expanded in morphology and increased in number. This may be because the excessive proliferation of malignant cells in the body has a greater demand for energy, which stimulates the growth of mitochondria in the body. Compared with the model group, the mitochondrial structure of the gastric mucosa of the rats in the YQHY group, especially the YQHY-H group, was destroyed ( Figure 7 ), these results suggest that YQHY can effectively destroy the structure of mitochondria in the gastric mucosa of CAG rats, damage mitochondria, and thus prevent the proliferation of malignant cells in the gastric mucosa of CAG rats.

[0178] 4) The ATP detection kit detects ATP in gastric mucosal tissue and analyzes it with a luminometer. First, the tissue is fully lysed to release the ATP in the tissue; then, according to the requirements of the ATP detection kit instructions, the lysate is mixed with the reaction mixture in the kit, which contains firefly luciferase and its substrate. In the presence of ATP, luciferase catalyzes the substrate to produce a light signal; then, the mixed reaction solution is quickly transferred to the detection dish of the luminometer, the instrument parameters are set, and the detection program is started; finally, the luminometer detects the light signal intensity in the reaction solution and converts it into a numerical value of ATP concentration, thereby quantitatively analyzing the content of ATP in the cell.

[0179] The results showed that compared with the model group, the ATP signal was significantly decreased after YQHY intervention ( Figure 8 ), indicating that mitochondria were damaged. This result shows that YQHY treats CAG by damaging mitochondria.

[0180] 5) Low levels of ROS and increased oxidative stress may damage the gastric mucosa and lead to the development of cancer. In contrast, elevated levels of intracellular ROS can lead to apoptosis of cancer cells and precancerous cells, showing the dual role of intracellular ROS (Chatterjee and Chatterjee, 2020). To further determine the number of apoptotic cells and the level of ROS in rat gastric mucosal tissue, we used TUNEL staining to mark apoptosis. TUNEL staining, or terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, is a method for detecting apoptosis that combines the technology of detecting reactive oxygen species (ROS) to determine the number of apoptotic cells and the level of ROS in rat gastric mucosal tissue. During the operation, the rat gastric mucosal tissue was first fixed, dehydrated, embedded, and cut into thin slices, which were then attached to a slide. Next, the slices were dewaxed and hydrated, treated with proteinase K to expose the ends of the DNA fragments, and then incubated in a TUNEL reaction mixture containing terminal deoxynucleotidyl transferase and labeled dUTP. During the incubation process, the DNA break ends of apoptotic cells were labeled to form a positive signal. The results showed that compared with the model group, the green fluorescence signal of the YQHY group was significantly enhanced, indicating that the apoptosis rate in rat tissues increased significantly after Chinese medicine intervention ( Fig. 9 The results showed that YQHY could effectively promote apoptosis of gastric mucosal malignant cells in CAG rats, thereby treating CAG.

[0181] We further labeled PCNA and KI-67 positive cells in the gastric mucosa by IHC. We analyzed the changes in the location and number of proliferation and apoptotic cells in the crypts of the gastric epithelial glands. The results showed that compared with the model group, the proliferation level in the YQHY group was significantly reduced ( Fig.10 , Fig.11 ). These results suggest that elevated ROS levels may lead to the proliferation and malignancy of gastric precancerous cells. However, YQHY can reduce the level of proliferation and induce apoptosis of CAG malignant cells, thereby hindering the further development of CAG.

[0182] 6) Immunofluorescence is a highly sensitive technique for detecting specific molecules in cells and tissues. In this study, we used immunofluorescence to measure the level of reactive oxygen species in the gastric mucosa of rats. Reactive oxygen species are highly reactive molecules that play an important role in physiological and pathological processes such as cell signaling and inflammatory responses. When mitochondria are damaged, ROS levels increase. In the experiment, we divided the rats into a control group, a model group, a YQHY low-dose treatment group, and a YQHY high-dose treatment group.

[0183] The results showed that the level of reactive oxygen in the gastric mucosa of rats in the control group was relatively stable, and the fluorescence signal was weak. Compared with the control group, the level of reactive oxygen in the gastric mucosa of rats in the model group was significantly increased due to specific pathological stimulation, which was manifested by a significant increase in the green fluorescence signal. This result indicates that the degree of oxidative stress in the gastric mucosa of rats in the model group is aggravated, which may lead to cell damage and inflammatory response. Further studies found that after the YQHY treatment group was given YQHY drug intervention, the level of reactive oxygen in the gastric mucosa of rats in the YQHY treatment group increased compared with the model group, and the green fluorescence signal was significantly enhanced ( Fig.12 ). This result indicates that YQHY can induce excessive accumulation of ROS in malignant cells of gastric mucosa of CAG rats, thereby promoting mitochondrial apoptosis and treating CAG.

[0184] 7) In this study, we used LC3 fluorescent antibody staining to detect the content and distribution of autophagosomes in rat gastric mucosal tissue. LC3 (microtubule-associated protein 1 light chain 3) is a key marker protein for autophagosome formation, and its expression level can directly reflect changes in autophagic activity. During the experiment, we first fixed and permeabilized the gastric mucosal tissue, then stained it with a specific LC3 fluorescent antibody, and observed and photographed it under a fluorescence microscope.

[0185] Through observation under a fluorescence microscope, we can clearly see the distribution of autophagosomes in the gastric mucosal tissue of rats in each group. The results showed that compared with the control group, the red fluorescence signal in the gastric mucosal tissue of rats in the model group was enhanced. This phenomenon indicates that the formation and accumulation of autophagosomes in the model group rats increased significantly, which may be due to the enhanced autophagic activity of gastric mucosal cells in pathological conditions in order to maintain their own homeostasis. Further analysis found that compared with the model group, the red fluorescence signal in the gastric mucosal tissue of rats in the YQHY treatment group was significantly enhanced ( Fig.13 ). This result shows that YQHY can effectively damage the mitochondria of rat gastric mucosal malignant cells, suggesting that YQHY can promote mitochondrial autophagy, damage mitochondria, and thus induce apoptosis of gastric mucosal malignant cells in CAG rats, achieving the effect of treating CAG.

[0186] 8) Through the Western blot analysis experiment, we analyzed the FOXO3 protein in each group. First, make the gel. Select a clean glass plate, and then prepare the lower layer of gel: select the formula ratio according to the thickness of the plate, fill it with anhydrous ethanol and press it flat. Wait for 10min+ to solidify, then pour out the anhydrous ethanol and dry the upper layer with filter paper. After preparing the upper layer of gel, add the next layer of gel to fill it up, and then immediately insert the comb. Wait for 10min+ to solidify. After the gel is successfully made, put the box into the electrophoresis instrument to prepare for sample loading. Then prepare the marker and sample. After taking out the refrigerator, the marker needs to be kept at low temperature, and the sample needs to be thawed in a metal bath. Next, prepare the electrophoresis solution: a total of 500mL is required, 5Xrunning:dd water=100mL:400mL. After pouring the electrophoresis solution into the electrophoresis box, add the sample, unplug the comb, and calculate the sample loading position according to the number of groups and the number of repetitions. Add 2μL of marker, and the sample volume is loaded according to the BCA result. The electrophoresis voltage is 90v, the time is 30min, and when the protein runs together and runs into the lower layer of gel, the voltage is 140v, the time is 40min, and when the protein runs to the bottom layer, prepare for transfer. Soak the sponge filter paper in the recycled transfer solution in advance. The PDVF membrane is cut into 8cm long and 5.5cm wide, and pre-activated with anhydrous ethanol. Turn off the electrophoresis instrument, take out the box, take out the board and put it in the transfer solution recycled last time. Pry open the short board, scrape off the upper pink glue, cut the contact between the two sides of the membrane and the board in the transfer solution, and then gently put the glue on the soaked sponge filter paper, spread the PDVF membrane, cover the upper filter paper sponge, clamp the clip, and the black is stuck in the red box. Pour the transfer solution: 1000mL is required, 5Xtransfer200mL+anhydrous ethanol200mL+dd water600mL. Take a basin, put 4 large ice cubes, put the electrophoresis instrument in it, add water, and put 1 small ice cube in the electrophoresis instrument. Align the electrodes and cover the lid, battery 270mA, 60min. When the time is up, recover the transfer solution. Take out the membrane and place it in the blocking solution for 30min (blocking solution: 30mLTBST+1.5g skim milk powder). After blocking, wash the milk with TBST, cut the membrane according to the molecular weight of the target protein, mark the band to be used in the upper left corner, and then incubate the primary antibody in the refrigerator at 4℃ overnight (the primary antibody is diluted according to the instructions), recover the primary antibody the next day, wash three times with TBST, shake at 50 speed, 5min each time, wash clean, add secondary antibody, incubate at room temperature on a shaker for 1h, recover the secondary antibody after 1h, wash three times with TBST (5min each time, shake at about 50), prepare the exposure solution, take A and B exposure solutions according to the amount of 100ul per strip, the ratio is 1:1. Take out the strip, dip it in water, spread it on the exposure meter plate with the front side facing up, drop the exposure liquid on the strip, close the door, and expose.

[0187] By western blot analysis, we found that YQHY treatment reduced the protein level of FOXO3 ( Fig.14). The results showed that in vivo, YQHY could inhibit the FOXO3 pathway and thus reverse the progression of CAG.

[0188] 9) We further detected the content of FOXO3 in gastric mucosal tissue by immunohistochemistry, and found that YQHY treatment reduced the content of FOXO3 ( Fig.15 ). The results showed that in vivo, YQHY could inhibit the FOXO3 pathway and thus reverse the progression of CAG.

[0189] 4. Cell experiments

[0190] (1) Construction and identification of CAG cell model

[0191] Normal human gastric epithelial cells GES-1 were induced into CAG precancerous cells (MC cells) with MNNG (25 μM) for 24 h and then subcultured normally for 2 generations.

[0192] (2) Cell grouping and drug administration

[0193] MC cells were used as the control group, and different doses of serum containing Yiqi Huayu Jiedu method were used for intervention to observe its effects on MC cell mitochondria, energy metabolism and malignant behavior of MC cells. The specific groups were as follows: ① control group, ② positive drug group (Buprofezin), ③ YQHY-H group, and ④ YQHY-L group.

[0194] (3) Index measurement and analysis

[0195] 1) CCK8 kit (Biyuntian Biotechnology) was used for cell viability detection. (5×103) cells were seeded in a 96-well plate, and after the cells adhered to the wall, different concentrations of YQHY were added for 24h and 48h. After that, the supernatant was removed, and the CCK8 solution was injected into the cells, and the cells were placed in a light-proof cell culture incubator for 1 to 2h. After the incubation, the OD value of the cells at 450nm was measured using an ELISA instrument, and the cell viability was determined based on the OD value.

[0196] The results showed that compared with the control group, the number of MC cells in the positive drug group was significantly reduced. Compared with the positive drug group, the number of MC cells in the YQHY treatment group, especially the YQHY high-dose group, was significantly reduced ( Fig.16 ). These results indicate that YQHY drug has a significant damaging effect on MC cells.

[0197] 2) Plate cloning experiment calculates the clone formation rate of each group of cells and analyzes their proliferation ability. Cell cloning experiment is a delicate cell biology technique, whose main purpose is to separate single cells with specific characteristics from the original cell population and obtain a group of cells with the same genetic background through asexual reproduction. This process involves multiple steps. The first is the separation of cells. We use trypsin enzymatic hydrolysis to release cells from the culture dish and disperse them into a suspension of single cells. Next, in order to ensure that there are only a small number of cells in each culture container, we perform limiting dilution of the cell suspension and inoculate the cells into the culture dish at a very low density (5000 / well). After inoculation, the cells will grow in a specific cell culture medium containing nutrients such as essential amino acids, vitamins, minerals, growth factors and serum, and will be placed in a constant temperature incubator to maintain an appropriate temperature and carbon dioxide concentration to simulate the growth environment of cells in vivo. After a period of culture, single cells will begin to divide and proliferate, eventually forming cell clones visible to the naked eye. Finally, staining and photography are performed.

[0198] The results showed that compared with the control group, the MC cell clones in the positive drug group were significantly reduced, and the number of clones was significantly reduced. Compared with the positive drug group, the MC cell clones in the YQHY treatment group, especially the YQHY high-dose group, were significantly reduced, and the number of clones was significantly reduced ( Fig.17 ). These results indicate that YQHY drug can effectively reduce the proliferation ability of MC cells.

[0199] 3) Transwell detection of changes in cell invasion ability in each group. When conducting cell Transwell experiments, first, we prepared the Transwell chamber and selected the appropriate pore size according to the experimental requirements to ensure the simulation accuracy of cell migration or invasion. Then, the Transwell insert plate and the collection plate were placed in the upper chamber and the lower chamber respectively, and pre-warmed, serum-free culture medium was added between the two chambers to eliminate the interference of serum components on cell migration. Then the cells were digested with trypsin and resuspended in culture medium containing serum. After adjusting the cell density, a certain number of cells were inoculated into the upper chamber. After the cells adhered to the wall, the culture medium in the upper chamber was gently removed, and the cells were exposed to serum-free culture medium to start the migration or invasion process. After the set culture time, the Transwell chamber was carefully removed, the non-migrated cells were wiped off with a cotton swab, and then the Transwell chamber was fixed, stained and transparentized. Finally, the cells that migrated to the lower surface of the filter membrane were observed and photographed under a microscope, and the migration or invasion ability of the cells was evaluated by counting and analysis.

[0200] The results showed that compared with the control group, the invasive ability of MC cells in the positive drug group was significantly reduced. Compared with the positive drug group, the invasive ability of MC cells in the YQHY treatment group, especially the YQHY high-dose group, was significantly reduced ( Fig.18 ). These results indicate that YQHY drug can effectively reduce the invasive ability of MC cells.

[0201] 4) The apoptosis kit was used to stain each group of cells, and the results of cell apoptosis were detected by flow cytometry. In the experiment, each group of cells was first digested with trypsin and collected into a centrifuge tube, and washed twice with pre-cooled PBS to remove impurities; then, according to the instructions of the apoptosis kit, the cells were resuspended in binding buffer, and appropriate amounts of AnnexinV-FITC and PI staining agents were added, gently mixed and incubated in the dark for 15-20 minutes; after staining, the cell sample was immediately placed in the detection tube of the flow cytometer, and the cells were subjected to dual-color fluorescence detection by adjusting the detection parameters of the instrument, and the fluorescent signals of FITC and PI were used to distinguish between live cells, early apoptotic cells and late apoptotic cells, and finally the quantitative detection results of cell apoptosis were obtained.

[0202] The results showed that compared with the control group, the number of MC apoptosis increased after YQHY intervention ( Fig.19 ). This result indicates that YQHY drug can effectively damage MC cells to treat CAG.

[0203] 5) The cycle kit is used to stain each group of cells, and the cell cycle results are detected by flow cytometry. First, each group of cell samples is prepared into a single cell suspension to ensure that the cell concentration meets the requirements of flow cytometry detection. Next, according to the operating instructions of the cycle kit, the cell suspension is mixed with the dyes in the kit, including propidium iodide (PI) and ribonuclease (RNase), which can specifically bind to cell DNA. In the dark, the mixed cell suspension is incubated at room temperature for a period of time, usually 15-30 minutes, to allow the dye to fully enter the cells and bind to DNA. After the incubation is completed, the stained cell suspension is transferred to the sample tube of the flow cytometer and prepared for detection. On the flow cytometer, first set the appropriate detection parameters, including the excitation wavelength of the laser, the detection channel of the fluorescence signal, and the parameters of the scattered light. Start the flow cytometer and let the cell suspension pass through the detection area in the form of a single cell. The laser beam will excite the PI dye bound to the DNA to produce a specific fluorescence signal. Flow cytometry divides cells into different cycle stages according to the different DNA content of cells, mainly including G0 / G1 phase, S phase and G2 / M phase. The DNA content of G0 / G1 phase cells is diploid, the DNA content of S phase cells is between diploid and tetraploid, and the DNA content of G2 / M phase cells is tetraploid. Flow cytometry assigns cells to corresponding cycle stages by analyzing the fluorescence intensity of each cell and calculates the proportion of cells in each cycle stage.

[0204] Finally, data were collected using specialized flow cytometry analysis software, and the results were statistically analyzed to compare differences in the cell cycle among the groups.

[0205] The results showed that compared with the control group, the G2 / M phase of MC cells was significantly enhanced after YQHY intervention ( Fig. 20 ), indicating that YQHY enhanced the cycle arrest of CAG. This result shows that YQHY drug can effectively damage MC cells to treat CAG.

[0206] 6) Each group of cells was stained with Mito-Tracker Green, and mitochondrial damage was analyzed using a laser confocal microscope. In this experiment, we used Mito-Tracker Green, a specific mitochondrial dye, to stain each group of cells. This dye can effectively mark mitochondria in living cells and give them a bright green fluorescence. During the staining process, we strictly followed the concentration and time recommended in the instructions to ensure that the dye can fully enter the cells and bind to the mitochondria. Subsequently, we used a high-resolution laser confocal microscope to conduct a detailed analysis of the stained cells. By adjusting the parameters of the microscope, we can clearly observe the changes in the morphology, distribution, and fluorescence intensity of the mitochondria, so as to accurately assess the degree of mitochondrial damage in each group of cells under experimental conditions.

[0207] The results showed that the green fluorescence signal in the positive drug intervention group was significantly weakened compared with the control group. Further research found that the green fluorescence signal in the YQHY treatment group, especially the YQHY high-dose intervention group, was significantly weakened after the YQHY drug intervention ( Fig.21 ). This result indicates that YQHY drug can effectively damage MC cell mitochondria to treat CAG.

[0208] 7) Each group of cells was stained with the JC-1 kit, and the changes in mitochondrial membrane potential were observed under a laser confocal microscope. In this study, we used the JC-1 kit to stain each group of cells to detect and observe the changes in mitochondrial membrane potential. JC-1 is a widely used mitochondrial membrane potential indicator that can form different aggregates in cells according to the difference in membrane potential, thereby emitting different fluorescence signals. In the experiment, we strictly followed the operating steps provided by the kit to ensure the standardization of the staining process and the reliability of the results. First, we incubated each group of cells with JC-1 dye under appropriate conditions so that JC-1 could enter the cells and bind to the inner membrane of the mitochondria. In healthy mitochondria, JC-1 mainly exists in the form of polymers and emits strong red fluorescence; while in mitochondria with reduced membrane potential, JC-1 exists in the form of monomers and emits green fluorescence. Therefore, by observing the ratio of red to green fluorescence in the cell, we can judge the state of mitochondrial membrane potential. Next, we used a laser confocal microscope to observe the stained cells in detail. Under the microscope, we can clearly see the distribution of mitochondria in the cell and the fluorescence signal of the JC-1 dye. By adjusting the laser intensity and detector sensitivity of the microscope, we were able to capture subtle differences in changes in mitochondrial membrane potential. These differences were visually displayed through changes in fluorescence color, with a decrease in red fluorescence and an increase in green fluorescence indicating a drop in mitochondrial membrane potential, a hallmark of cellular damage.

[0209] The results showed that compared with the control group, the green fluorescence in the positive drug group was enhanced and the red fluorescence was weakened. Compared with the positive drug group, the green fluorescence in the YQHY drug intervention group, especially the YQHY high-dose intervention group, was significantly enhanced and the red fluorescence was significantly weakened ( Fig. 22 ). This result indicates that YQHY can damage MC cell mitochondria, thereby damaging MC cells and treating CAG.

[0210] 8) The ATP detection kit detects cellular ATP and analyzes it with a luminometer. First, add the cell lysate to the cell sample to be tested to ensure that the cells are fully lysed and release the ATP in the cell; then, according to the requirements of the ATP detection kit instructions, mix the lysate with the reaction mixture in the kit, which contains firefly luciferase and its substrate. In the presence of ATP, luciferase catalyzes the substrate to produce a light signal; then, quickly transfer the mixed reaction solution to the detection dish of the luminometer, set the instrument parameters, and start the detection program; finally, the luminometer detects the light signal intensity in the reaction solution and converts it into a numerical value of ATP concentration, thereby quantitatively analyzing the content of ATP in the cell.

[0211] The results showed that compared with the control group, the ATP signal was significantly decreased after YQHY intervention ( Fig.23 ). This result suggests that YQHY damages mitochondria, leading to reduced ATP production, thereby treating CAG.

[0212] 9) DCFH-DA was used to stain each group of cells, and the ROS levels of each group of cells were observed and analyzed under a fluorescence microscope. The DCFH-DA fluorescent probe was diluted and added to each group of cell culture dishes. The MC cells were incubated at 37°C and 5% CO2 for 30-60 minutes. DCFH-DA entered the cells and was converted into DCFH. The cells were then washed with PBS to remove the probe that did not enter the cells. Under a fluorescence microscope, the fluorescence signal of DCF in the cells was observed at an excitation wavelength of 485nm and an emission wavelength of 530nm. The average fluorescence intensity of each group of cells was quantified by image analysis software to analyze and compare the ROS levels in each group of cells.

[0213] The results showed that the green fluorescence signal of the positive drug intervention group was significantly enhanced compared with the control group. Further studies found that the green fluorescence signal of the YQHY treatment group, especially the YQHY high-dose intervention group, was significantly enhanced ( Fig.24 ). This result indicates that YQHY can induce excessive accumulation of ROS in MC cells, damage MC cell mitochondria, and promote MC cell apoptosis to treat CAG.

[0214] 10) Mito-Tracker Red CMXRos red dye was used to detect the level of ROS in cell mitochondria. In this experiment, we used Mito-Tracker Red CMXRos, a specific mitochondrial dye, to dye each group of cells. During the staining process, we strictly followed the concentration and time recommended in the instructions to ensure that the dye could fully enter the cells. The average fluorescence intensity of each group of cells was quantified by image analysis software to analyze and compare the level of ROS in each group of cells.

[0215] The results showed that compared with the control group, the red fluorescence signal of the positive drug intervention group was significantly enhanced. Further research found that the red fluorescence signal of the YQHY treatment group, especially the YQHY high-dose intervention group, was significantly enhanced ( Fig.25 ). This result indicates that YQHY can promote the accumulation of ROS in MC cells, damage MC cell mitochondria, and promote MC cell apoptosis to treat CAG.

[0216] 11) Through the Western blot analysis experiment, we analyzed the FOXO3 protein in each group. First, make the gel. Select a clean glass plate, and then prepare the lower layer of gel: select the formula ratio according to the thickness of the plate, fill it with anhydrous ethanol and press it flat. Wait for 10min+ to solidify, then pour out the anhydrous ethanol and dry the upper layer with filter paper. After preparing the upper layer of gel, add the next layer of gel to fill it up, and then immediately insert the comb. Wait for 10min+ to solidify. After the gel is successfully made, put the box into the electrophoresis instrument to prepare for sample loading. Then prepare the marker and sample. After taking out the refrigerator, the marker needs to be kept at low temperature, and the sample needs to be thawed in a metal bath. Next, prepare the electrophoresis solution: a total of 500mL is required, 5Xrunning:dd water=100mL:400mL. After pouring the electrophoresis solution into the electrophoresis box, add the sample, unplug the comb, and calculate the sample loading position according to the number of groups and the number of repetitions. Add 2ul of marker, and the sample volume is added according to the BCA result. The electrophoresis voltage is 90v, the time is 30min, and when the protein runs together and runs into the lower layer of gel, the voltage is 140v, the time is 40min, and when the protein runs to the bottom layer, prepare for transfer. Soak the sponge filter paper in the recycled transfer solution in advance. The PDVF membrane is cut into 8cm long and 5.5cm wide, and pre-activated with anhydrous ethanol. Turn off the electrophoresis instrument, take out the box, take out the board and put it in the transfer solution recycled last time. Pry open the short board, scrape off the upper pink glue, cut the contact between the two sides of the membrane and the board in the transfer solution, and then gently put the glue on the soaked sponge filter paper, spread the PDVF membrane, cover the upper filter paper sponge, clamp the clip, and the black is stuck in the red box. Pour the transfer solution: 1000mL is required, 5Xtransfer200mL+anhydrous ethanol200mL+dd water600mL. Take a basin, put 4 large ice cubes, put the electrophoresis instrument in it, add water, and put 1 small ice cube in the electrophoresis instrument. Align the electrodes and cover the lid, battery 270mA, 60min. When the time is up, recover the transfer solution. Take out the membrane and place it in the blocking solution for 30min (blocking solution: 30mLTBST+1.5g skim milk powder). After blocking, wash the milk with TBST, cut the membrane according to the molecular weight of the target protein, mark the band to be used in the upper left corner, and then incubate the primary antibody in the refrigerator at 4℃ overnight (the primary antibody is diluted according to the instructions), recover the primary antibody the next day, wash three times with TBST, shake at 50 speed, 5min each time, wash clean, add secondary antibody, incubate at room temperature on a shaker for 1h, recover the secondary antibody after 1h, wash three times with TBST (5min each time, shake at about 50), prepare the exposure solution, take A and B exposure solutions according to the amount of 100ul per strip, the ratio is 1:1. Take out the strip, dip it in water, spread it on the exposure meter plate with the front side facing up, drop the exposure liquid on the strip, close the door, and expose.

[0217] By western blot analysis, we found that YQHY treatment reduced the protein level of FOXO3 ( Fig.26). The results showed that in vivo, YQHY could inhibit the FOXO3 pathway and thus reverse the progression of CAG.

[0218] In the description of this specification, specific features, structures, materials or characteristics may be combined in an appropriate manner in any one or more embodiments or examples.

[0219] The above is only a specific embodiment of the present invention, but the protection scope of the present invention is not limited thereto. Any person skilled in the art can easily think of changes or substitutions within the technical scope disclosed by the present invention, which should be included in the protection scope of the present invention. Therefore, the protection scope of the present invention should be based on the protection scope of the claims.

Claims

1. A Chinese medicine composition for treating chronic atrophic gastritis, characterized in that: The invention comprises the following raw materials in parts by weight: 2-30 parts of astragalus, 2-30 parts of atractylodes, 1-30 parts of codonopsis, 1-30 parts of tuckahoe, 1-30 parts of yam, 1-40 parts of salvia, 2-30 parts of trifoliate gracile, 1-40 parts of curcuma, 1-20 parts of costusroot, 1-20 parts of amomum, 2-30 parts of tangerine peel, 1-30 parts of pinellia, 1-30 parts of dried ginger, 5-20 parts of coptis, 1-30 parts of immature bitter orange, 3-30 parts of chicken's gizzard lining and 2-30 parts of raw licorice.

2. A Chinese medicine composition for treating chronic atrophic gastritis according to claim 1, characterized in that: The invention comprises the following raw materials in parts by weight: 5-25 parts of astragalus, 10-30 parts of atractylodes, 5-25 parts of codonopsis, 3-28 parts of tuckahoe, 3-26 parts of yam, 2-35 parts of salvia, 5-25 parts of trifoliate gracile, 2-36 parts of zedoaria, 3-18 parts of costusroot, 4-18 parts of amomum, 5-28 parts of tangerine peel, 5-25 parts of pinellia, 3-30 parts of dried ginger, 5-18 parts of coptis, 5-30 parts of immature bitter orange, 5-30 parts of chicken's gizzard lining and 5-25 parts of raw licorice.

3. A Chinese medicine composition for treating chronic atrophic gastritis according to claim 1, characterized in that: The invention comprises the following raw materials in parts by weight: 5-20 parts of astragalus, 12-28 parts of atractylodes, 8-25 parts of codonopsis, 5-25 parts of tuckahoe, 5-24 parts of yam, 5-30 parts of salvia, 5-20 parts of trifoliate radix, 3-35 parts of zedoaria, 5-15 parts of costusroot, 5-15 parts of amomum, 5-25 parts of tangerine peel, 5-20 parts of pinellia, 4-25 parts of dried ginger, 5-15 parts of coptis, 5-25 parts of immature bitter orange, 5-20 parts of chicken's gizzard lining and 5-20 parts of raw licorice.

4. A Chinese medicine composition for treating chronic atrophic gastritis according to claim 1, characterized in that: The invention comprises the following raw materials in parts by weight: 10-20 parts of astragalus, 15-20 parts of atractylodes, 10-20 parts of codonopsis, 10-25 parts of tuckahoe, 10-20 parts of yam, 10-20 parts of salvia, 5-15 parts of trifoliate gracile, 5-30 parts of curcuma, 5-10 parts of costusroot, 5-10 parts of amomum, 5-20 parts of tangerine peel, 5-15 parts of pinellia, 4-20 parts of dried ginger, 5-10 parts of coptis, 5-15 parts of immature bitter orange, 10-20 parts of chicken's gizzard lining and 5-10 parts of raw licorice.

5. A Chinese medicine composition for treating chronic atrophic gastritis according to claim 1, characterized in that: The invention comprises the following raw materials in parts by weight: 20 parts of astragalus, 15 parts of atractylodes, 20 parts of codonopsis, 15 parts of tuckahoe, 15 parts of yam, 10 parts of salvia miltiorrhiza, 5 parts of trillium, 5 parts of curcuma, 6 parts of costusroot, 6 parts of amomum, 6 parts of tangerine peel, 10 parts of pinellia, 5 parts of dried ginger, 5 parts of coptis, 6 parts of immature bitter orange, 15 parts of chicken's gizzard lining, and 6 parts of raw licorice.

6. A method for preparing a Chinese medicine composition for treating chronic atrophic gastritis according to any one of claims 1 to 5, characterized in that: The following steps are involved: S1: Weigh astragalus, atractylodes, codonopsis, tuckahoe, yam, salvia, sparganium, curcuma, costusroot, amomum, tangerine peel, pinellia, dried ginger, coptis, immature bitter orange, chicken gizzard lining and raw liquorice according to weight ratio and set aside; S2: Mix the Chinese medicinal materials in S1, add 10 to 20 times the weight of the medicinal materials in water, soak for 0.5 to 1 hour, decoct twice, each time for 0.5 to 1 hour, filter the decoction twice, discard the residue, and keep the decoction for later use.

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