Composition for protecting gastric mucosa, relieving gastroenteritis and promoting peristalsis and application thereof

Abstract

The invention provides a composition for protecting gastric mucosa, relieving gastroenteritis and promoting peristalsis and application of the composition, and particularly relates to a composition which comprises hericium erinaceus or an extract of the hericium erinaceus, Chinese yam or an extract of the Chinese yam and rhizoma zingiberis or an extract of the rhizoma zingiberis. The composition can remarkably improve gastrointestinal motility, repair gastrointestinal mucosa injury and relieve gastrointestinal inflammation. The liquid dairy product containing the composition is harmonious in taste, unique in flavor and high in acceptability of audiences.

Description

Technical Field

[0001] The present invention relates to the field of functional foods or medicines, and in particular to a composition for protecting gastric mucosa, relieving gastrointestinal inflammation and promoting peristalsis, and its application. Background Art

[0002] With the influence of factors such as the accelerated pace of life, increased mental stress and bad living habits, stomach problems have become a key issue concerning people's quality of life and even their health. Among them, indigestion, chronic gastritis (chronic inflammation of the gastric mucosa caused by various causes, including chronic non-atrophic gastritis and chronic atrophic gastritis), flatulence, abdominal discomfort and other symptoms are the most prominent. The occurrence of these symptoms is often related to drinking, improper diet, low immunity, Helicobacter pylori infection and the like. As the mucosal layer of the stomach, the gastric mucosa has a strong defense ability and plays an important role in maintaining the physiological function of the stomach. When its defense factors are weakened or the invasion factors are enhanced, it can lead to gastric mucosal damage, and then cause the occurrence of chronic gastritis. Alternatively, when the gastric mucosa is stimulated by chronic uncontrollable inflammation for a long time, it will produce a large amount of inflammatory mediators, which further induce normal cell proliferation, and eventually lead to cell gene mutations, inducing the occurrence and development of gastric cancer.

[0003] Currently, the improvement and treatment of gastric problems, especially gastric mucosal damage, still mainly relies on drugs, including prokinetics, nonsteroidal anti-inflammatory drugs, acid suppressants, and anti-Helicobacter pylori drugs. Compared with Western medicine treatments that are prone to side effects such as dependence, nausea, and diarrhea, Chinese herbal components or compositions have advantages in improving human health, such as more ingredients, more targets, higher safety, and fewer toxic side effects. For example, Lizhong Decoction, Shenling Baizhu San, and Sijunzi Decoction are all classic Chinese herbal prescriptions for regulating the spleen and stomach and warming and strengthening the body. However, most Chinese herbal prescriptions have complex components and poor taste, and are less accepted by the general population. In addition, the medicinal materials in Chinese herbal prescriptions cannot be added to ordinary foods, which seriously limits their application in functional foods.

[0004] Furthermore, some patients with chronic gastritis are not sensitive to medication. A poor diet may be a key factor in the inefficiency of drug treatment, and appropriate dietary regulation is crucial. Although there is no clear evidence linking a causal relationship between dietary intake and the development of chronic gastritis symptoms, dietary changes and lifestyle adjustments are integral to the treatment of chronic gastritis. Currently, clinicians often advise patients to avoid long-term, high-dose use of medications that can damage the gastric mucosa (such as NSAIDs) and to improve their diet and lifestyle.

[0005] Therefore, it is of great significance to provide food or health food that is beneficial to gastric health (eg, improving or assisting in the treatment of gastric diseases or symptoms). Summary of the Invention

[0006] The present invention provides a composition comprising food-derived plants or their extracts. Compared to individual components, the components of the composition synergistically inhibit gastrointestinal inflammation, improve gastrointestinal motility, and repair gastric mucosal damage. The composition can be used in foods, health foods, functional foods, foods for special medical purposes, and nutritional formulas, and has broad application prospects.

[0007] Specifically, the present invention provides a composition comprising Hericium erinaceus or an extract thereof, Chinese yam or an extract thereof, and dried ginger or an extract thereof.

[0008] In some embodiments, the composition further comprises an oligopeptide. As used herein, an oligopeptide refers to an oligopeptide having a molecular weight of less than 1000 Daltons and consisting of 2-10 amino acids. In some embodiments, the oligopeptide is selected from soybean oligopeptides, walnut oligopeptides, wheat oligopeptides, and corn oligopeptides, preferably wheat oligopeptides.

[0009] In some embodiments, the composition comprises, by weight, 1-20 parts of Hericium erinaceus extract, 3-15 parts of Dioscorea opposita extract, and 1-10 parts of Dried Zingiber officinale extract.

[0010] In some embodiments, the composition comprises 3-10 parts of Hericium erinaceus extract, 5-15 parts of Dioscorea opposita extract, and 3-10 parts of Zingiber officinale extract.

[0011] In some embodiments, the composition includes 4-8 parts of Hericium erinaceus extract, 6-12 parts of Dioscorea opposita extract, and 4-8 parts of Zingiber officinale extract.

[0012] In some embodiments, the composition comprises, by weight, 1-20 parts of Hericium erinaceus extract, 5-20 parts of yam extract, 1-10 parts of dried ginger extract, and 0.5-5 parts of oligopeptides.

[0013] In some embodiments, the composition includes 1-10 parts of Hericium erinaceus extract, 5-12 parts of yam extract, 2-10 parts of dried ginger extract, and 0.5-2 parts of oligopeptides.

[0014] In some embodiments, the composition includes 2-10 parts of Hericium erinaceus extract, 5-10 parts of yam extract, 3-8 parts of dried ginger extract, and 0.5-1.5 parts of oligopeptides.

[0015] In some embodiments, the composition includes 3-8 parts of Hericium erinaceus extract, 8-10 parts of yam extract, 4-8 parts of dried ginger extract, and 1 part of oligopeptide.

[0016] In some embodiments, the composition includes 3-9 parts of Hericium erinaceus extract, 8-10 parts of yam extract, 4-8 parts of dried ginger extract, and 1 part of oligopeptide.

[0017] In some embodiments, the polysaccharide content in the Hericium erinaceus extract is ≥0.15%. The polysaccharide content of some Hericium erinaceus extract products can be as high as 6.8% to 15.6% after further concentration and purification.

[0018] In some embodiments, the polysaccharide content in the yam extract is ≥0.08%. The polysaccharide content of some yam extract products can be as high as 0.23% to 3.13% after further concentration and purification.

[0019] In some embodiments, the dried ginger extract has a 6-gingerol content of (80 mg / 100 g to 150 mg / 100 g).

[0020] In some embodiments, the wheat oligopeptides have a protein content of >90%, oligopeptides of >70%, and glutamine of >18%.

[0021] The extracts in the present invention can be prepared by extraction or purchased.

[0022] In some embodiments, the Hericium erinaceus extract can be prepared by the following method: using Hericium erinaceus as raw material, and obtaining it through water extraction, centrifugation, separation, concentration, sterilization and other operations.

[0023] In some embodiments, the Chinese yam extract can be prepared by the following method: using Chinese yam as raw material, homogenizing, centrifuging, adding auxiliary material maltodextrin, sterilizing, etc.

[0024] In some embodiments, the dried ginger extract can be prepared by the following method: using dried ginger as raw material, and obtaining it through water extraction, centrifugation, membrane separation, concentration, sterilization, spray drying and the like.

[0025] In some embodiments, whole milk is used to extract and dry ginger to obtain the dried ginger extract. In some embodiments, whole milk powder is dissolved in deionized water at a mass ratio of 5% to 20% to obtain the whole milk, and the dried ginger and the whole milk are mixed at a ratio of 1: (5-50) (for example, 1: (15-25), and another example is 1: 20), and the extraction is carried out under the following conditions: extraction temperature 20-95 ° C (for example, 40-95 ° C, and another example is 70 ° C), stirring time 10 min to 24 h (for example, 15 min-1.5 h, and another example is 1 h), stirring speed 100-1000 rpm, freeze drying 24-72 h, thereby obtaining the dried ginger extract. The biologically active substances in the dried ginger extract obtained by this method are greatly improved.

[0026] In some embodiments, the dried ginger extract is the emulsified dried ginger described in CN118177371A, which is obtained by extracting dried ginger using an emulsified fat composition. The entire contents of CN118177371A are incorporated herein by reference.

[0027] In some embodiments, the wheat oligopeptide can be prepared by the following method: using wheat gluten as raw material, and using enzymatic hydrolysis to obtain a powdered sample with oligopeptides having a relative molecular weight less than 1000U as the main component, thereby obtaining the wheat oligopeptide.

[0028] In some embodiments, the composition is a powder, granules, pills, paste, or liquid preparation.

[0029] In another aspect, the present invention provides a food comprising the composition according to any one of the first aspect.

[0030] In some embodiments, the food contains 0.1 to 10% of the composition by weight.

[0031] In some embodiments, the food product is selected from the group consisting of dairy products, beverages, confectionery products, condiments, and meat products.

[0032] In some embodiments, the dairy product is selected from liquid dairy products (eg, ambient temperature liquid dairy products or low temperature liquid dairy products), cheese, yogurt, milk flakes, and milk powder.

[0033] In some embodiments, the candy is selected from chocolate, hard candy, soft candy, ice cream, popsicles, baked desserts (such as cookies, cakes, egg tarts) and fried desserts.

[0034] In some embodiments, the beverage is selected from the group consisting of a solid beverage, a semi-solid beverage, and a liquid beverage (eg, juice, soda).

[0035] In some embodiments, the noodle product is selected from baked noodle products (bread, pizza, pancakes) and steamed noodle products (steamed buns, flower rolls, and dumplings).

[0036] In some embodiments, the condiment is selected from milk cap, decorating sauce, food sauce and coating powder.

[0037] In some embodiments, the meat product is selected from cured meat (eg, bacon, ham), canned meat (eg, luncheon meat), and raw meat (eg, sashimi).

[0038] In some embodiments, the food product is a dairy product, such as liquid dairy product or milk powder.

[0039] In some embodiments, the food is a health food.

[0040] In some embodiments, the health food is in the form of tablets, powders, granules, teas, granules, pills, pastes, hard capsules, soft capsules, oral liquids, beverages, wines, syrups or drops.

[0041] The health care products mentioned in the present invention refer to foods with health care (functions), which have the common properties of general foods, can regulate the functions of the human body, and are suitable for consumption by specific groups of people, but are not intended to treat diseases.

[0042] In another aspect, the present invention provides use of the composition of any one of the first aspect or the food of any one of the second aspect in the preparation of a medicine or a health food, wherein the medicine is used to prevent and / or treat gastric diseases or symptoms; and the health food is used to improve or assist in the treatment of gastric diseases or symptoms.

[0043] In some embodiments, the present invention provides the use of the composition or food in preparing a product for improving or assisting in the treatment of gastric diseases or symptoms. The product may be the aforementioned food or health product (health food) of the present invention, or may be used to prepare other types of food or health products.

[0044] In some embodiments, the gastric disease or condition is selected from gastric mucosal damage, gastrointestinal inflammation (eg, chronic non-atrophic gastritis or chronic atrophic gastritis), and gastrointestinal hypomotility.

[0045] In the present invention, "treating" means reversing, alleviating the progression of the disease to which it is applied, or one or more symptoms of the disease.

[0046] In some embodiments, the improvement or adjunctive treatment of gastric diseases or symptoms includes improving one or more of the following symptoms:

[0047] Improve weight indicators in patients with gastric diseases;

[0048] Improve food and / or water intake in patients with gastric disorders;

[0049] Improve the shedding of mucosal epithelium in patients with gastric diseases;

[0050] Improve gastrin levels;

[0051] Improve the secretion level of prostaglandin E2;

[0052] Improve the levels of pepsinogen I (PGI) and / or pepsinogen II (PGII);

[0053] Improve the levels of pepsinogen I (PGI) and / or pepsinogen II (PGII);

[0054] Improve serum VEGF (Vascular Endothelial Growth Factor) levels;

[0055] Improve the expression levels of oxidative stress and inflammatory factors; the oxidative stress and inflammatory factors include one or more of MDA (Malondialdehyde), SOD, IL-6, IFN-γ, and TNF-α.

[0056] The present invention provides a composition comprising Hericium erinaceus or an extract thereof, Chinese yam or an extract thereof and dried ginger or an extract thereof, wherein the composition may further contain oligopeptides. Compared with a single ingredient, the composition can significantly improve the effects of inhibiting gastrointestinal inflammation, improving gastrointestinal motility, and repairing gastric mucosal damage, and has a synergistic effect. In addition, the composition can be applied to ordinary foods. For example, dairy products (milk powder, cheese, liquid milk, etc.) to which the composition is added have a good taste and flavor compared to unadded products or similar commercially available products (stomach-nourishing products), and are highly accepted by the test population. BRIEF DESCRIPTION OF THE DRAWINGS

[0057] The accompanying drawings are used to provide a further understanding of the present invention and constitute a part of the present invention. The exemplary embodiments of the present invention and the accompanying drawings are used to explain the present invention and do not constitute an improper limitation of the present invention. In the accompanying drawings:

[0058] Figure 1 : Analysis results of fluorescence intensity of the gastrointestinal tract of each group of zebrafish in Effect Example 1.

[0059] Figure 2 : Example photos of the gastrointestinal tract of each group of zebrafish in Effect Example 1 under a fluorescence microscope.

[0060] Figure 3 : Analysis results of gastrointestinal tract area of ​​zebrafish in each group in Effect Example 2.

[0061] Figure 4 : Example photos of the gastrointestinal tract of each group of zebrafish in Effect Example 2 under a dissecting microscope.

[0062] Figure 5 : Statistical results of the number of neutrophils in the gastrointestinal tract of zebrafish in each group in Effect Example 3.

[0063] Figure 6 : Example pictures showing the number of neutrophils in the gastrointestinal tract of each group of zebrafish in Effect Example 3 under a fluorescence microscope.

[0064] Figure 7 It shows that the product of the present invention improves the oral administration dose of each group in the experiment of chronic gastritis in rats.

[0065] Figure 8 Shows the changes in body weight of experimental animals during the modeling process.

[0066] Figure 9 Shows the changes in food intake of experimental animals during the modeling process.

[0067] Figure 10 Shows the changes in water intake of experimental animals during the modeling process.

[0068] Figure 11 Shows the changes in animal body weight during the intervention experiment.

[0069] Figure 12 Shows the changes in animal feed intake during the intervention experiment.

[0070] Figure 13 Shows the changes in animals' water intake during the intervention experiment.

[0071] Figure 14 and Figure 15 Shows the results of pathological analysis of experimental animals.

[0072] Figure 16 Shows the results of gastrin secretion in experimental animals.

[0073] Figure 17 Shows the results of prostaglandin E2 testing in experimental animals.

[0074] Figure 18 Shows the results of pepsinogen I detection in experimental animals.

[0075] Figure 19 Shows the results of pepsinogen Ⅱ test in experimental animals.

[0076] Figure 20 Shows the MDA test results of experimental animals.

[0077] Figure 21 Displays the SOD test results of experimental animals.

[0078] Figure 22 Shows the TNF-α test results of experimental animals.

[0079] Figure 23 Shows the IL-6 test results of experimental animals.

[0080] Figure 24 Shows the VEGF detection results of experimental animals.

[0081] Figure 25 Shows the IFN-γ detection results of experimental animals. DETAILED DESCRIPTION

[0082] The embodiments of the present invention will be described in detail below with reference to the examples, but it will be understood by those skilled in the art that the following examples are merely illustrative of the present invention and should not be construed as limiting the scope of the invention. Where specific conditions are not specified in the examples, the methods were performed according to conventional conditions or the conditions recommended by the manufacturer. Where the manufacturers of the reagents or instruments are not specified, they are all conventional products that can be obtained commercially.

[0083] The raw materials in the present invention can be extracted by oneself (according to the method described above) or purchased.

[0084] The Hericium erinaceus extract is obtained by using Hericium erinaceus as raw material through water extraction, centrifugation, separation, concentration and sterilization. The Hericium erinaceus extract contains a polysaccharide component from Hericium erinaceus of ≥0.15%.

[0085] Chinese Yam Extract: Made from high-quality Chinese Yam, the extract is homogenized, centrifuged, supplemented with maltodextrin, and sterilized. The Chinese Yam Extract contains ≥0.08% polysaccharide from Chinese Yam.

[0086] Dried ginger extract: Dried ginger extract is obtained by extracting dried ginger with whole milk powder and then drying it (also known as milk-extracted dried ginger extract). This method significantly increases the bioactive content of the dried ginger extract. The dried ginger extract contains ≥80mg / 100g of 6-gingerol.

[0087] Wheat oligopeptides: A powdered sample produced from wheat gluten using an enzymatic hydrolysis method, with oligopeptides having a relative molecular weight of less than 1000 U as the main component. The wheat oligopeptides contain >90% protein, >70% oligopeptides, and >18% glutamine.

[0088] Example 1

[0089] 7 parts by mass of Hericium erinaceus extract, 7 parts by mass of yam extract, and 7 parts by mass of dried ginger extract were uniformly mixed according to the above parts by mass to obtain a composition.

[0090] Example 2

[0091] 5.25 parts by mass of Hericium erinaceus extract, 10.5 parts by mass of yam extract, and 5.25 parts by mass of dried ginger extract were uniformly mixed according to the above parts by mass to obtain a composition.

[0092] Example 3

[0093] 8 parts by mass of Hericium erinaceus extract, 8 parts by mass of yam extract, 4 parts by mass of dried ginger extract, and 1 part by mass of wheat oligopeptide were uniformly mixed to obtain a composition.

[0094] Example 4 Liquid dairy product containing a composition for protecting gastric mucosa, relieving gastrointestinal inflammation and promoting peristalsis

[0095] Preparation method: Heat pasteurized milk to 50-55°C, add weighed composition of Example 3 and stabilizer, wherein the amount of composition of Example 3 added is 0.8% (i.e., its content in the liquid dairy product), and stir for 15-25 minutes using a stirrer with shearing and dispersing functions; then homogenize using a primary pressure of 30-50 bar and a secondary pressure of approximately 200 bar, while controlling the temperature at 50-55°C; and ultra-high temperature sterilize at 137-143°C / 4 seconds to obtain the liquid dairy product.

[0096] Example 5 Solid beverage containing a composition for protecting gastric mucosa, relieving gastrointestinal inflammation and promoting peristalsis

[0097] Preparation method: The composition prepared in Example 1 is mixed with a fruit and vegetable juice flavoring, wherein the added amount of the composition in Example 1 is 8.25% (i.e., its content in the solid beverage), and each raw material is sieved through a 40-mesh sieve and then mixed to prepare the product.

[0098] Comparative Example 1

[0099] In this comparative example, only Hericium erinaceus extract was used.

[0100] Comparative Example 2

[0101] In this comparative example, only the Chinese yam extract was used.

[0102] Comparative Example 3

[0103] This comparative example used only the dried ginger extract.

[0104] Comparative Example 4

[0105] In this comparative example, only wheat oligopeptides were used.

[0106] Comparative Example 5

[0107] In this comparative example, 8 parts by mass of Hericium erinaceus extract, 8 parts by mass of yam extract, 4 parts by mass of Poria cocos extract, and 1 part by mass of wheat oligopeptide were used, and the raw materials were uniformly mixed according to the above parts by mass to obtain a composition.

[0108] Comparative Example 6

[0109] This comparative example provides a functional liquid dairy product, the preparation method of which is as follows: heating pasteurized milk to 50-55°C, adding dried ginger extract of the same mass as that in Example 4, and stirring for 15-25 minutes using a stirrer with shearing and dispersing functions; then homogenizing with a primary pressure of 30-50 BAR and a secondary pressure of about 200 BAR, and controlling the temperature at 50-55°C; and ultra-high temperature sterilization at 137-143°C / 4s to obtain the liquid dairy product.

[0110] Effect Example 1 Gastrointestinal motility improvement efficacy evaluation experiment

[0111] (1) Experimental samples

[0112] Samples prepared in Examples 1 to 3 and Comparative Examples 1 to 5.

[0113] (2) Experimental animals

[0114] Wild-type AB strain zebrafish: Breeding was performed using natural pair mating. Zebrafish were 3 days post-fertilization (dpf), with 30 fish per experimental group. This was used to evaluate the efficacy of the drug in improving gastrointestinal motility and repairing gastrointestinal mucosal damage.

[0115] Zebrafish were reared in aquaculture water at 28°C (water quality: 200 mg of instant sea salt per liter of reverse osmosis water, conductivity 450-550 μS / cm; pH 6.5-8.5; hardness 50-100 mg / L CaCO3). They were bred and provided by the Hangzhou Huante Biotechnology Co., Ltd. Fish Farming Center, and their husbandry and management met the requirements of the international AAALAC accreditation.

[0116] (3) Instruments and reagents

[0117] Dissecting microscope (SZX7, OLYMPUS, Japan); CCD camera (VertA1, Shanghai Tusen Vision Technology Co., Ltd., China); motorized focus continuous zoom fluorescence microscope (AZ100, Nikon, Japan); precision electronic balance (CP214, OHAUS, USA); 6-well plate (Nest Biotech, China); dimethyl sulfoxide (DMSO, batch number BCCD8942, Sigma, Switzerland); trinitrobenzenesulfonic acid (TNBS, batch number SLCK4178, Sigma, USA); methylcellulose (batch number C2004046, Shanghai Aladdin Biochemical Technology Co., Ltd., China); Nile red (batch number SLBP9326V, Sigma, India).

[0118] (4) Experimental methods

[0119] Gastrointestinal motility improvement efficacy experiment: 3dpf wild-type AB strain zebrafish were randomly selected and plated in 6-well plates, with 30 zebrafish treated in each well (experimental group). Except for the normal control group, all other experimental groups were given TNBS in water to establish a zebrafish indigestion model. After 2 days of treatment at 28°C, TNBS was removed and Nile red was given in water as a fluorescent indicator of intestinal contents. After feeding, the zebrafish were randomly assigned to 6-well plates, with 30 zebrafish treated in each well (experimental group). The comparative example group and the example group were both treated with the drug at a dose concentration of 110μg / mL. A normal control group and a model control group were also set up, with the volume of each well being 3mL. After treatment at 28°C until 7dpf, 8 zebrafish were randomly selected from each group and photographed under a fluorescence microscope. The images were saved and analyzed and collected using NIS-Elements D 3.20 advanced image processing software. The zebrafish gastrointestinal fluorescence intensity (S) was analyzed and statistically analyzed to evaluate the gastrointestinal motility improvement efficacy of the samples.

[0120] (5) Experimental results (Table 1, Figure 1-Figure 2 )

[0121] Table 1 Gastrointestinal motility improvement test results after treatment with the test sample (n=8)

[0122] Group Gastrointestinal fluorescence intensity (pixels) Gastrointestinal motility improvement rate (%) Normal control group 243588±11332a Model control group 515823±19505f Positive control group (domperidone) 231198±14942a Comparative Example 1 472340±31867ef 15.97 Comparative Example 2 429974±17097de 31.53 Comparative Example 3 414561±8891cd 37.20 Comparative Example 4 419823±9900cde 35.26 Comparative Example 5 420964±14361cde 34.84 Example 1 360252±21725b 57.15 Example 2 367902±19013bc 54.34 Example 3 359387±14134b 57.46

[0123] Effect Example 2 Gastrointestinal mucosal damage repair efficacy evaluation experiment

[0124] (1) Experimental samples

[0125] Samples prepared in Examples 1 to 3 and Comparative Examples 1 to 5.

[0126] (2) Experimental animals

[0127] Same as Experimental Example 1.

[0128] (3) Instruments and reagents

[0129] Same as Experimental Example 1.

[0130] (4) Experimental methods

[0131] Evaluation of the repair efficacy of gastrointestinal mucosal damage: 3dpf wild-type AB strain zebrafish were randomly selected in a 6-well plate, and 30 zebrafish were treated in each well (experimental group). Except for the normal control group, the other experimental groups were given water-soluble TNBS to establish a zebrafish gastrointestinal mucosal damage model. After 2 days of treatment at 28°C, TNBS was removed, and 30 zebrafish were treated in each well (experimental group). The comparative group and the embodiment group were both treated with a dosage concentration of 110μg / mL. At the same time, a normal control group and a model control group were set up, and the capacity of each well was 3mL. After continuing to treat at 28°C for 2 days, 8 zebrafish were randomly selected from each experimental group and placed under a dissecting microscope for photography. NIS-Elements D 3.20 advanced image processing software was used to collect data and analyze the zebrafish gastrointestinal tract area (A). The statistical analysis results of this indicator were used to evaluate the sample's gastrointestinal mucosal damage repair efficacy.

[0132] (5) Experimental results (Table 2, Figure 3-Figure 4 )

[0133] Table 2. Experimental results of gastrointestinal mucosal damage repair after treatment with test samples (n=8)

[0134] Group Gastrointestinal tract area (pixels) Gastrointestinal tract area repair rate (%) Normal control group 36936±1363a Model control group 66246±2579g Positive control group (prednisone) 48059±2094bcd 62.05 Comparative Example 1 52324±2097cde 47.50 Comparative Example 2 57921±2213ef 28.40 Comparative Example 3 59512±2654f 22.98 Comparative Example 4 51857±881cde 49.09 Comparative Example 5 53555±1903def 43.30 Example 1 46115±3472bc 68.68 Example 2 44260±1945b 75.01 Example 3 41273±2465ab 85.20

[0135] Effect Example 3: Gastrointestinal Inflammation Relief Efficacy Evaluation Experiment

[0136] 1. Experimental samples

[0137] Samples prepared in Examples 1-3 and Comparative Examples 1-5.

[0138] 2. Experimental Animals

[0139] Transgenic neutrophil fluorescent zebrafish (MPX): Zebrafish aged 3 dpf were used to evaluate the efficacy of the sample in alleviating gastrointestinal inflammation.

[0140] 3. Instruments and Reagents

[0141] Same as Experimental Example 1.

[0142] 4. Experimental Methods

[0143] Gastrointestinal inflammation relief efficacy experiment: 3dpf transgenic neutrophil green fluorescent zebrafish were randomly selected in a 6-well plate, and 30 zebrafish were treated in each well (experimental group). Except for the normal control group, the other experimental groups were given water-soluble TNBS to establish a zebrafish gastrointestinal mucosal injury model. After 2 days of treatment at 28°C, TNBS was removed, and 30 zebrafish were treated in each well (experimental group). The control group and the embodiment group were treated with a dosage concentration of 110μg / mL, and a normal control group and a model control group were set up at the same time, with a capacity of 3mL per well. After continuing to treat at 28°C for 2 days, 8 zebrafish were randomly selected from each experimental group and photographed under a fluorescence microscope using NIS-Elements D

[0144] 3.20 Advanced image processing software was used to collect data and analyze the number of neutrophils (N) in the zebrafish gastrointestinal tract. The statistical analysis results of this indicator were used to evaluate the efficacy of the sample in alleviating gastrointestinal inflammation.

[0145] (5) Experimental results (Table 3, Figure 5-Figure 6 )

[0146] Table 3. Experimental results of the effect of the test article on the improvement of the number of neutrophils (n=8)

[0147] Group Number of neutrophils Inflammation improvement rate (%) Normal control group 5.8±0.37a Model control group 16.0±1.25e Positive control group (prednisone) 6.5±0.33a 92.68 Comparative Example 1 9.5±0.42b 63.41 Comparative Example 2 11.5±0.46cd 43.90 Comparative Example 3 11.8±0.56d 41.46 Comparative Example 4 10.0±0.73bc 58.54 Comparative Example 5 9.6±0.42b 62.20 Example 1 6.6±0.50a 91.46 Example 2 6.8±0.49a 90.24 Example 3 6.1±0.30a 96.34

[0148] Effect Example 4 Sensory Evaluation of Liquid Dairy Products

[0149] The liquid dairy products of Example 4 and Comparative Example 6 were stored at 4°C, 25°C, and 37°C, and their sensory properties were evaluated after 1 month, 3 months, and 6 months under accelerated conditions. The evaluation criteria are shown in Table 4, and the results are shown in Table 5.

[0150] Table 4 Comprehensive evaluation standards for sensory indicators

[0151] index Evaluation Criteria Score weight Appearance The color is milky white or slightly yellow, uniform and without stratification 20 Organizational form Uniform and fine texture, without whey separation 25 Taste The taste is delicate and smooth, with milk, ginger and sweet taste 30 Flavor Rich milk flavor with ginger aroma 25

[0152] Table 5 Sensory evaluation results of liquid dairy products

[0153]

[0154]

[0155] The sensory evaluation results showed that Example 4 had a higher overall score than Comparative Example 7 as the storage time prolonged, and Comparative Example 6 began to show obvious loss of ginger flavor after 3 months of storage, and the taste was not harmonious; while Example 4 was able to retain the aroma of ginger to a greater extent under the ratio of the composition, and the overall audience acceptance was higher.

[0156] Effect Example 5: Test results of product improving chronic gastritis in rats

[0157] Male Sprague-Dawley rats (180 ± 20 g) were used for the experiment, with eight rats per group. After seven days of adaptive feeding, rats were given MNNG (170 μg / ml) for drinking and an irregular diet (one full day of fasting followed by one day of feeding). MNNG (170 μg / ml, 1 ml / 100 g) was then administered orally every other day for 10 weeks to establish the model. Two rats were randomly selected from each treatment group, and gastric tissue pathological changes were observed to confirm successful model establishment. After model establishment, the corresponding functional raw materials were administered orally once daily for four weeks.

[0158] The oral doses for each group are shown in Figure 7 Among them, the formula milk 1, formula milk 2 and formula milk 3 are obtained by adding Hericium erinaceus extract, Chinese yam extract, lactic acid dried ginger extract and wheat oligopeptide extract to the existing base milk in proportion.

[0159] The detection indicators include: basic indicators: body weight, food intake, and water intake; gastric juice biochemical indicators: gastric juice volume, gastric acidity, and pepsin; gastric mucosal pathology indicators: chronic inflammation score, mucosal thickness, and the number of intrinsic glands; serum biochemical indicators: gastrin-17, pepsinogen I, pepsinogen II, vascular endothelial growth factor, and prostaglandin E2; oxidative stress and inflammatory factors: IL-6, IFN-γ, TNF-α, MDA, and SOD.

[0160] Modeling experiment results Figures 8-10 .

[0161] Figure 8 The figure shows the weight changes of experimental animals during modeling. It can be seen that the blank control group's weight increased steadily, while the model group's weight increased more slowly than the normal group. Twelve weeks after modeling, the average weight of rats in the normal group was 505.17g, while the average weight of rats in the model group was 319.91g.

[0162] Figure 9 The figure shows the changes in the experimental animals' feed intake during the modeling process. It can be seen that the normal group's feed intake steadily increased after modeling. The model group's feed intake reached its maximum in the sixth week of modeling and then declined in the seventh week.

[0163] Figure 10 The figure shows the changes in water intake of experimental animals during modeling. It can be seen that water intake in the normal group increased steadily after modeling. Water intake in the model group reached its maximum in the sixth week of modeling and then decreased in the seventh week.

[0164] Intervention trial results Figure 11-Figure 25 .

[0165] Figure 11The data shows changes in animal weight during the intervention experiment. It can be seen that the blank control group showed steady weight gain, while the model group showed slower weight gain than the normal and intervention groups. After four weeks of intervention, the average weight of rats in the normal group was 526.18g, the average weight of rats in the model group was 403.3g, the average weight of rats in the positive control group was 419.22g, the average weight of rats in Formula 1 was 422.1g, the average weight of rats in Formula 2 was 421.6g, the average weight of rats in Formula 3 was 425.3g, and the average weight of the basic milk group was 405.16g.

[0166] Figure 12 The figure shows the changes in animal feed intake during the intervention experiment. The figure shows a steady increase in feed intake in the normal group after the intervention. During the four-week intervention period, the model group had the lowest feed intake, while the intervention group had the highest feed intake in the other groups.

[0167] Figure 13 The figure shows changes in water intake during the intervention experiment. The figure shows a steady increase in water intake in the normal group after the intervention. During the four-week intervention period, the model group had the lowest water intake, while the intervention group had the highest water intake among the other groups.

[0168] Figure 14 and Figure 15 The results of pathological analysis of experimental animals are shown. In the blank control group, obvious mucosal layer, submucosa, muscularis, and serosa structures can be seen. In the model control group, the epithelium of the muscularis mucosa was shed, the glandular glands atrophied, and the muscularis and lower layers shed. In the positive control group, local epithelial detachment of the mucosal layer was observed, and a complete gastric glandular structure was visible, with a relatively regular distribution of the glandular glands. In the low-dose group of the present invention, the epithelium of the mucosal layer was shed, the glandular glands atrophied, and the glandular glands were relatively regularly distributed. There was local separation between the muscularis mucosa and the muscularis, and local loss of the muscularis. In the medium-dose group of the present invention, local epithelial detachment of the mucosal layer was observed, a complete gastric glandular structure was visible, local glandular glands atrophied, and the glandular glands were relatively regularly distributed. In the high-dose group of the present invention, a small amount of epithelial detachment of the mucosal layer was observed, no inflammatory cell infiltration was observed, a complete gastric glandular structure was visible, and the glandular glands were regularly distributed. In the basic milk group, the epithelial detachment of the mucosal layer was observed, gastric mucus secretion was high and exuded, inflammatory cells infiltrated in the mucosal layer, and the glandular structure was locally atrophied. Pathological results showed that MNNG and an irregular diet induced gastric mucosal epithelial cell shedding, shedding of cells in the upper mucosal layer, atrophy or reduction of the intrinsic glands, and irregular distribution of the intrinsic glands. Compared with the model group, Formula 3 showed less epithelial cell shedding in the mucosal layer, more complete and regular arrangement of the intrinsic glands, and was more effective than the other groups.

[0169] Figure 16The results of gastrin secretion in experimental animals are shown. Gastrin is mainly secreted by G cells in the gastric antrum and is an important gastrointestinal hormone. Under normal circumstances, gastrin can promote the secretion of hydrochloric acid by gastric parietal cells to help digest food. Too low gastrin levels may be related to lesions such as gastric mucosal atrophy. Atrophic gastric mucosa will lead to a decrease in gastrin-secreting cells. Gastrin can not only promote the secretion of gastric acid and pepsin, but also regenerate the gastric mucosa, improve gastrointestinal motility, and accelerate gastric emptying. In the present invention, there are significant differences between the control group and the model group, and the differences are statistically significant (P < 0.01), indicating that the modeling is successful. Compared with the model group, the gastrin content in the positive control group was significantly increased, and the differences were statistically significant (P < 0.01), the gastrin content in formula three was significantly increased, and the differences were statistically significant (P < 0.01), and the gastrin content in formula two was significantly increased, and the differences were statistically significant (P < 0.01). There was no significant difference between formula 2 and formula 3 and the blank control group, but there was a significant difference between formula 1 and the blank control group, indicating that the anti-inflammatory effects of formulas 2 and 3 were better than those of formula 1.

[0170] Figure 17 The results of prostaglandin E2 detection in experimental animals are shown. In the rat atrophic gastritis model, prostaglandin E2 (PGE2) is an important substance. Prostaglandin E2 is a metabolite of arachidonic acid and belongs to the prostaglandin family. In normal gastric mucosa, PGE2 plays a role in protecting the gastric mucosa. It can increase the blood flow to the gastric mucosa, promote the secretion of gastric mucosal mucus and bicarbonate, and help maintain the integrity of the gastric mucosa. In rat atrophic gastritis, changes in the content of PGE2 reflect the damage and repair status of the gastric mucosa. If the PGE2 level decreases, it means that the protective mechanism of the gastric mucosa is weakened, and gastritis may be further aggravated. Because atrophic gastritis destroys the normal structure of the gastric mucosa, it reduces the cells that produce PGE2, thereby reducing its secretion. In the present invention, there are significant differences between the control group and the model group, and the differences are statistically significant (P < 0.01), indicating that the modeling is successful. Compared with the model group, the serum PGE2 content of rats treated with Formula 3 was significantly increased, with the differences being statistically significant (P < 0.01). The serum PGE2 content of rats treated with Formula 2 was also significantly increased, with the differences being statistically significant (P < 0.01). There were no significant differences between Formulas 2 and 3 and the blank control group, while there was a significant difference between Formula 1 and the blank control group, indicating that Formulas 2 and 3 were more effective in reducing inflammation than Formula 1.

[0171] Figure 18The results of pepsinogen I testing in experimental animals are shown. In studies of chronic atrophic gastritis in rats, pepsinogen I (PGI) is an important biomarker that reflects the functional state of the gastric mucosa, especially the activity of gastric chief cells. Pepsinogen is a precursor of pepsin and is mainly secreted by the chief cells of the fundic glands. PGI is converted into active pepsin under the action of gastric acid and participates in protein digestion. The level of PGI is closely related to the functional state of the gastric mucosa, especially the secretory function of the fundic glands. In chronic atrophic gastritis in rats, a decrease in PGI levels reflects the atrophy and functional impairment of the gastric mucosal glands and is an important indicator for assessing the severity of the disease and gastric acid secretion function. In the present invention, the PGI concentration in the positive control group was significantly higher than that in the model control group (p<0.05), indicating that the gastric mucosal damage in the positive control group was milder and PGI secretion was higher. The PGI concentrations in the low-dose group, the medium-dose group, and the high-dose group were all significantly lower than that in the positive control group (p<0.05), indicating that these dose treatments did not have the same protective effect on the gastric mucosa as the positive control group. There was no significant difference in PGⅠ concentration between the high-dose group and the positive control group (p>0.05), indicating that the high-dose treatment may have an antioxidant effect similar to that of the positive control group.

[0172] Figure 19 The results of pepsinogen II assays in experimental animals are shown. Pepsinogen II is a precursor of pepsin, primarily secreted by the chief cells of the fundic glands and the pyloric gland cells of the gastric antrum. Unlike PG I, PG II secretion is not limited to the fundic glands and can therefore be detected in different regions of the gastric mucosa (fundus and antrum). PG II is converted into active pepsin by gastric acid and participates in protein digestion. Although PG II secreting cells are widely distributed, PG II levels may decrease in cases of severe gastric mucosal atrophy. Unlike PG I, a decrease in PG II usually occurs later because the pyloric glands in the gastric antrum may be relatively preserved in the early stages of atrophic gastritis. In the present invention, the PG II concentration in the positive control group was significantly higher than that in the model control group (p < 0.05), indicating that the gastric mucosal damage in the positive control group was milder and PG II secretion was higher. PG II concentrations in the low-dose, medium-dose, and high-dose groups were all significantly lower than those in the positive control group (p < 0.05), indicating that these doses did not protect the gastric mucosa as well as the positive control group. The PGII concentrations in the low-dose and medium-dose groups were significantly lower than those in the positive control group (p<0.05), while the PGII concentration in the high-dose group was not significantly different from that in the positive control group (p>0.05), indicating that the effect of the high-dose group was better than that of the low-dose and medium-dose groups.

[0173] Figure 20The results of MDA test on experimental animals are shown. MDA (Malondialdehyde) is one of the end products of lipid peroxidation. When polyunsaturated fatty acids in the cell membrane are attacked by free radicals, lipid peroxidation occurs, generating MDA. MDA is a highly active molecule that can react with biomacromolecules such as proteins and DNA, causing cell damage. The level of MDA is generally used to assess the degree of oxidative stress and oxidative damage to tissues. In chronic atrophic gastritis in rats, elevated MDA levels reflect the degree of oxidative stress and lipid peroxidation damage in the gastric mucosa, and are important indicators for assessing the severity of the disease and the therapeutic effect. In the present invention, the MDA content of the positive control group was significantly higher than that of the blank control group (p<0.05), but lower than that of the model control group (p<0.05), indicating that a certain degree of oxidative stress existed in the positive control group. The MDA content of the low-dose group, the medium-dose group, and the high-dose group were all significantly lower than that of the model control group (p<0.05), indicating that these formulas all have a certain antioxidant effect. The MDA content in the low-dose and medium-dose groups was significantly higher than that in the positive control group (p<0.05), while the MDA content in the high-dose group was not significantly different from that in the positive control group (p>0.05), indicating that the antioxidant effect of the high-dose group may be better than that of the low-dose and medium-dose groups.

[0174] Figure 21 Displays the SOD test results of experimental animals. SOD (Superoxide Dismutase) is a key antioxidant enzyme that can catalyze superoxide free radicals (O2 - ) is converted into hydrogen peroxide (H2O2) and oxygen (O2), thereby scavenging free radicals and reducing oxidative stress. SOD is an important component of the body's antioxidant defense system and is widely present in the cytoplasm, mitochondria and extracellular fluid. In rats with chronic atrophic gastritis, a decrease in SOD activity reflects a decline in the antioxidant capacity of the gastric mucosa and an aggravation of oxidative stress, and is an important indicator for assessing the severity of the disease and the therapeutic effect. In the present invention, the SOD activity of the positive control group was significantly higher than that of the model control group (p<0.05), indicating that the positive control group had a higher antioxidant capacity. The SOD activity of the low-dose group and the medium-dose group was significantly lower than that of the positive control group (p<0.05), but higher than that of the model control group, indicating that the low-dose and medium-dose treatments had a certain effect on improving SOD activity, but not as good as the positive control group. There was no significant difference in SOD activity between the high-dose group and the positive control group (p>0.05), indicating that the high-dose treatment may have an antioxidant effect similar to that of the positive control group.

[0175] Figure 22The results of TNF-α detection in experimental animals are shown. TNF-α (Tumor Necrosis Factor-alpha, tumor necrosis factor-α) is a proinflammatory cytokine mainly produced by macrophages, monocytes and T cells. It plays an important role in inflammatory response, immune regulation and cell apoptosis. TNF-α activates downstream signaling pathways (such as NF-κB and MAPK pathways) by binding to its receptors (TNFR1 and TNFR2), inducing the release of inflammatory mediators and cell damage. In chronic atrophic gastritis in rats, increased TNF-α levels reflect the intensity of the inflammatory response and the degree of damage to the gastric mucosa, and are important indicators for assessing the severity of the disease and the therapeutic effect. In the present invention, there was a significant difference between the control group and the model group (P<0.05), indicating that the model was successfully established. There was a significant difference between the intervention group and the model group (P<0.05), indicating that the functional factor has a certain anti-inflammatory effect. The TNF-α level in the low-dose group was significantly higher than that in the positive control group (p<0.05), indicating that the anti-inflammatory effect of the low-dose group was not as good as that of the positive control group. The TNF-α level in the medium-dose group was similar to that in the positive control group, indicating that the medium dose has a certain anti-inflammatory effect. The TNF-α level in the high-dose group was significantly lower than that in the positive control group (p < 0.05), indicating that the high-dose group had a better anti-inflammatory effect than the positive control group. The TNF-α level in the basic milk group was significantly higher than that in the positive control group (p < 0.05), indicating that the basic milk group had a weaker anti-inflammatory effect than the positive control group.

[0176] Figure 23 The results of IL-6 detection in experimental animals are shown. IL-6 (Interleukin-6) is a pleiotropic cytokine mainly produced by macrophages, T cells, B cells and fibroblasts. It plays an important role in inflammatory response, immunoregulation, cell proliferation and differentiation. IL-6 activates downstream signaling pathways (such as JAK / STAT and MAPK pathways) by binding to its receptor, inducing the release of inflammatory mediators and cellular responses. In chronic atrophic gastritis, the gastric mucosa is stimulated by multiple factors such as Helicobacter pylori infection, gastric acid reflux, and autoimmune response, leading to increased secretion of IL-6. Elevated IL-6 levels directly reflect the intensity of the inflammatory response of the gastric mucosa. In the present invention, there was a significant difference between the control group and the model group (P<0.05), indicating that the positive control group had a certain anti-inflammatory effect. There was a significant difference between the intervention group and the model group (P<0.05), indicating that the anti-inflammatory effects of these two groups were not as good as those of the positive control group. The IL-6 levels in the medium-dose and high-dose groups were significantly lower than those in the low-dose and basic milk groups (p<0.05), indicating that the two groups had certain anti-inflammatory effects, among which the high-dose group had the most significant effect, close to the level of the positive control group.

[0177] Figure 24The results of VEGF detection in experimental animals are shown. VEGF (Vascular Endothelial Growth Factor) is an important angiogenic factor, primarily produced by endothelial cells, macrophages, and epithelial cells. It promotes the proliferation, migration, and survival of vascular endothelial cells by binding to its receptors (VEGFR-1, VEGFR-2, etc.), thereby inducing the formation of new blood vessels. In the present invention, the VEGF concentration in the model group was significantly higher than that in the blank control group (p < 0.05), indicating that the model treatment successfully induced VEGF expression. The VEGF concentration in the positive control group was significantly lower than that in the model group (p < 0.05), indicating that the positive control drug effectively inhibited VEGF expression. The VEGF concentrations in the low-, medium-, and high-dose groups were also significantly lower than those in the model group (p < 0.05). However, compared with the positive control group, the VEGF concentrations in the low- and medium-dose groups were slightly higher, while the VEGF concentration in the high-dose group was similar to that in the positive control group, indicating that the high-dose group was more effective than the low- and medium-dose groups.

[0178] Figure 25 The results of IFN-γ detection in experimental animals are shown. IFN-γ (Interferon-gamma) is a cytokine mainly produced by Th1 cells, natural killer cells (NK cells) and cytotoxic T cells (CTL). It plays an important role in immune regulation, antiviral, anti-tumor and inflammatory responses. IFN-γ regulates the immune response by activating macrophages, enhancing antigen presentation and inducing the release of other inflammatory mediators. In chronic atrophic gastritis in rats, increased IFN-γ levels reflect the Th1 type immune response and inflammation intensity of the gastric mucosa, and are important indicators for assessing the severity of the disease and the therapeutic effect. In the present invention, compared with the model group, the IFN-γ concentration in the model group was significantly higher than that in the blank control group (p<0.05), indicating that the model successfully induced the expected immune response. Compared with the intervention group, the IFN-γ concentration in the positive control group was significantly lower than that in the model group (p<0.05), indicating that the positive control drug effectively inhibited the expression of IFN-γ. The IFN-γ concentrations in the low-, medium-, and high-dose groups were also significantly lower than those in the model group (p<0.05). However, compared with the positive control group, the IFN-γ concentrations in the low- and medium-dose groups were slightly higher, while the IFN-γ concentration in the high-dose group was similar to that in the positive control group, indicating that the effect of the high-dose group was better than that of the low- and medium-dose groups.

[0179] Although the specific embodiments of the present invention have been described in detail, it will be understood by those skilled in the art that various modifications and substitutions may be made to those details based on all the teachings disclosed, and these changes are all within the scope of protection of the present invention. The full scope of the present invention is given by the appended claims and any equivalents thereof.

Claims

1. A composition comprising Hericium erinaceus or an extract thereof, Chinese yam or an extract thereof, and dried ginger or an extract thereof.

2. The composition of claim 1, further comprising an oligopeptide; Preferably, the oligopeptide is selected from soybean oligopeptide, walnut oligopeptide, wheat oligopeptide and corn oligopeptide, more preferably wheat oligopeptide.

3. The composition of claim 1 or 2, comprising, by weight, 1-20 parts of Hericium erinaceus extract, 3-15 parts of Chinese yam extract, and 1-10 parts of dried ginger extract; Preferably, the composition comprises 3-10 parts of Hericium erinaceus extract, 5-15 parts of Chinese yam extract, and 3-10 parts of dried ginger extract; More preferably, the composition comprises 4-8 parts of Hericium erinaceus extract, 6-12 parts of Dioscorea opposita extract, and 4-8 parts of Zingiber officinale extract.

4. The composition of claim 2, comprising, by weight, 1-20 parts of Hericium erinaceus extract, 5-20 parts of Chinese yam extract, 1-10 parts of dried ginger extract, and 0.5-5 parts of oligopeptide; Preferably, the composition comprises 1-10 parts of Hericium erinaceus extract, 5-12 parts of Chinese yam extract, 2-10 parts of dried ginger extract, and 0.5-2 parts of oligopeptide; More preferably, the composition comprises 2-10 parts of Hericium erinaceus extract, 5-10 parts of Chinese yam extract, 3-8 parts of dried ginger extract, and 0.5-1.5 parts of oligopeptide; More preferably, the composition comprises 3-8 parts of Hericium erinaceus extract, 8-10 parts of Chinese yam extract, 4-8 parts of dried ginger extract, and 1 part of oligopeptide; or More preferably, the composition comprises 3-9 parts of Hericium erinaceus extract, 8-10 parts of yam extract, 4-8 parts of dried ginger extract, and 1 part of oligopeptide.

5. The composition according to any one of claims 1 to 4, wherein the dried ginger extract is obtained by extracting the dried ginger with 5-50 times the amount of whole milk (the whole milk is obtained by dissolving whole milk powder in water at a mass ratio of 5% to 20%) under the following conditions: extraction temperature of 20-95° C., stirring time of 10 min-24 h, stirring speed of 100-1000 rpm, and freeze-drying for 24-72 h.

6. The composition according to any one of claims 1 to 5, which is in the form of a powder, granules, pills, paste or liquid preparation.

7. A food comprising the composition according to any one of claims 1 to 6; Preferably, the food contains 0.1%-10% of the composition by weight.

8. The food of claim 7, wherein the food is selected from the group consisting of dairy products, beverages, flour products, condiments, and meat products; Preferably, the dairy product is selected from liquid dairy products (e.g., room temperature liquid dairy products or low temperature liquid dairy products), cheese, yogurt, milk flakes and milk powder; Preferably, the candies are selected from chocolate, hard candies, soft candies, ice cream, popsicles, baked desserts (such as biscuits, cakes, egg tarts) and fried desserts; Preferably, the beverage is selected from solid beverages, semi-solid beverages and liquid beverages (such as juices, sodas); Preferably, the noodle product is selected from baked noodle products (bread, pizza, pancakes) and steamed noodle products (steamed buns, flower rolls, dumplings); Preferably, the condiment is selected from milk cap, decoration sauce, food sauce and coating powder; Preferably, the meat product is selected from cured meat (such as bacon, ham), canned meat (such as luncheon meat) and raw meat (such as sashimi); Preferably, the food is a dairy product, such as liquid dairy product or milk powder.

9. The food according to claim 7 or 8, which is a health food; Preferably, the health food is in the form of tablets, powders, granules, teas, granules, pills, pastes, hard capsules, soft capsules, oral liquids, beverages, wines, syrups or drops.

10. Use of the composition according to any one of claims 1 to 6 or the food according to any one of claims 7 to 9 in the preparation of medicines or health foods, wherein: The medicine is used to prevent and / or treat gastric diseases or symptoms; the health food is used to improve or assist in the treatment of gastric diseases or symptoms; Preferably, the gastric disease or symptom is selected from gastric mucosal damage, gastrointestinal inflammation (eg, chronic non-atrophic gastritis) and gastrointestinal hypomotility.

11. Use of the composition according to any one of claims 1 to 6 or the food according to any one of claims 7 to 9 in preparing a product for improving or assisting in the treatment of gastric diseases or symptoms, such as a health food; Preferably, the gastric disease or symptom is selected from gastric mucosal damage, gastrointestinal inflammation (eg, chronic non-atrophic gastritis) and gastrointestinal hypomotility.

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