Human intestinal tract saliva combined lactobacillus Ligillaceus Salivarius MTR-1105 and application of human intestinal tract saliva combined lactobacillus Ligillaceus Salivarius MTR-1105

Abstract

The invention discloses a human intestinal tract combined lactobacillus salivarius MTR-1105 and an application of the human intestinal tract combined lactobacillus salivarius MTR-1105, and relates to the field of microorganisms, in particular to a human intestinal tract combined lactobacillus salivarius MTR-1105 and an application of the human intestinal tract combined lactobacillus salivarius MTR-1105. The strain preservation number of the lactobacillus unitus MTR-1105 is GDMCC (Grains Database Microorganism Center) 65345; the biological activity of the combined lactobacillus salivarius MTR-1105 is evaluated by further combining with an acute gastric mucosal injury rat model, and it is found that the combined lactobacillus salivarius MTR-1105 can inhibit gastric mucosal damage and bleeding induced by alcohol and non-steroidal anti-inflammatory drugs, down-regulate expression of inflammatory factors such as IL-6 and IL-1beta and generation of MDA, and up-regulate expression of antioxidant proteins such as CAT and SOD; the invention provides the lactobacillus salivarius combined MTR-1105 which can be used for preparing functional microbial agents, functional foods and medicines for protecting gastric mucosa, and has a wide application prospect.

Description

Technical Field

[0001] The present invention relates to the field of microorganisms, in particular to human intestinal saliva-associated lactobacillus (Ligilactobacillus salivarius) MTR-1105 and applications thereof. Background Art

[0002] Gastric mucosal injury refers to the destruction of gastric mucosal integrity caused by chemical factors (such as smoking, drinking, strong tea, coffee, and drugs that irritate the gastric mucosa such as aspirin, indomethacin, etc.), physical factors (excessive cold, excessive heat, overly rough food or overeating, etc.), and stimulation by bacteria or their toxins. Gastroscopy can show pathological changes such as changes in gastric mucosal color, bleeding, congestion, erosion, and ulcers. Gastric mucosal injury first manifests as the shedding and necrosis of the surface epithelium of the gastric mucosa caused by various pathogenic factors, resulting in superficial mucosal injury; further development of the injury can damage the microvascular endothelial cells, leading to mucosal ischemia, hypoxia, and tissue necrosis, resulting in deep mucosal injury (erosion or ulcer). Gastric mucosal injury usually causes gastrointestinal symptoms such as stomach pain, bloating, acid reflux, heartburn, nausea, and vomiting. If not treated in time, it may lead to gastritis, gastric ulcers, and even serious complications such as gastric bleeding and perforation. Due to the special physiological functions and physiological environment of the stomach, the repeated presence of stimuli such as food, microorganisms, and gastric acid leads to the continuous development of gastric mucosal damage, seriously affecting the patient's health level and quality of life.

[0003] Currently, mild gastric mucosal damage can be improved by removing pathogenic factors (such as eradicating Helicobacter pylori, discontinuing suspected drugs, correcting bad eating habits, etc.) and adjusting lifestyle (such as maintaining good living habits, regular work and rest, quitting smoking and limiting alcohol consumption, avoiding excessive fatigue and mental stress, etc.). For moderate to severe gastric mucosal damage, interventions such as drugs that inhibit gastric acid secretion and drugs that protect the gastric mucosa can be used to promote gastric mucosal repair. However, drug treatment has many adverse reactions and cannot be effective in the long term or prevent disease recurrence.

[0004] The gastrointestinal flora plays a crucial role in maintaining gastrointestinal homeostasis. A healthy and balanced gastrointestinal flora promotes food digestion, degrades foreign matter, and secretes mucin. This helps isolate toxic metabolites from the gastric mucosa, maintains intestinal immune balance, eliminates pathogens, and protects the gastric mucosa from various pathological factors. A variety of probiotics have been found to have protective effects on the gastric mucosa, but these strains are mostly isolated from the environment, plants, or animals. Human-derived microbiota are primarily found on the human body, in the oral cavity, and in the gastrointestinal tract. Through their long-standing symbiotic relationship with the human body, they have adapted to the body's relatively stable internal environment (such as temperature, pH, and nutritional conditions), developing specialized surface structures that facilitate colonization. Compared with non-human-derived microbiota, they are safer and more easily colonized. Lactobacillus salivarius is primarily found in oral saliva and can also be detected in the gastrointestinal tract. It produces lactase, which aids in the digestion and absorption of lactose. However, there are no reports or applications of Lactobacillus salivarius for protecting against gastric mucosal damage. The present invention provides a saliva-associated Lactobacillus MTR-1105 derived from the intestines of healthy humans. By integrating microbiological and pharmacological experimental techniques for the first time, we discovered that saliva-associated Lactobacillus MTR-1105 alleviates acute gastric mucosal damage in rats induced by alcohol and nonsteroidal anti-inflammatory drugs, demonstrating broad application prospects in clinical applications and functional food development. Summary of the Invention

[0005] The present invention provides a human intestinal saliva combined with Lactobacillus MTR-1105 and application thereof, so as to solve the problems existing in the above-mentioned prior art.

[0006] To achieve the above object, the present invention provides a human intestinal saliva-associated Lactobacillus MTR-1105, the strain deposit number of the saliva-associated Lactobacillus MTR-1105 is GDMCC 65345.

[0007] The present invention also provides an application of the saliva combined with Lactobacillus MTR-1105 in preparing a product for preventing and treating acute gastric mucosal damage.

[0008] Furthermore, the gastric mucosal damage is induced by chemical factors.

[0009] Furthermore, the gastric mucosal damage may be induced by alcohol or nonsteroidal anti-inflammatory drugs.

[0010] Furthermore, the chemical factors include alcohol or nonsteroidal anti-inflammatory drugs.

[0011] Furthermore, the strain form includes a cream form, a dry form, a freeze-dried form or a paste form.

[0012] Furthermore, a composition or derivative comprising the strain is selected from the group consisting of live bacteria, inactivated bacteria, freeze-dried bacterial powder, strain metabolites, bacterial lysates, or bacterial autolysates.

[0013] Furthermore, the composition is a functional bacterial agent (such as a probiotic preparation), a functional food or a medicine.

[0014] Furthermore, the functional bacterial agent is a probiotic preparation.

[0015] Furthermore, the functional food is in a solid, liquid, semi-solid or freeze-dried form.

[0016] Furthermore, the functional food is a health product, a special medical food, or a functional food.

[0017] Furthermore, the medicine also contains a pharmaceutically acceptable carrier.

[0018] The present invention discloses the following technical effects: The present invention isolates and identifies a saliva-associated Lactobacillus MTR-1105 from healthy human fecal samples. The present invention further evaluates its biological activity using a rat model of acute gastric mucosal injury and finds that saliva-associated Lactobacillus MTR-1105 can inhibit gastric mucosal damage and bleeding, downregulate the expression of inflammatory factors such as IL-6 and IL-1β and the production of peroxidation products such as MDA, and upregulate the expression of antioxidant proteins such as CAT and SOD, thereby preventing or treating acute gastric mucosal injury. The present invention not only clarifies the important role of this bacterium in acute gastric mucosal injury but also reveals its broad application prospects in the prevention and treatment of acute gastric mucosal injury. BRIEF DESCRIPTION OF THE DRAWINGS

[0019] In order to more clearly illustrate the embodiments of the present invention or the technical solutions in the prior art, the following briefly introduces the drawings required for use in the embodiments. Obviously, the drawings described below are only some embodiments of the present invention. For ordinary technicians in this field, other drawings can be obtained based on these drawings without paying any creative work.

[0020] Figure 1 The effect of saliva combined with Lactobacillus MTR-1105 on alcohol-induced gastric mucosal damage in rats in Example 2 (*, P < 0.05; ***, P < 0.001)

[0021] Figure 2 The effect of saliva combined with Lactobacillus MTR-1105 on alcohol-induced rat gastric mucosa HE and PAS staining in Example 2

[0022] Figure 3 The effect of saliva combined with Lactobacillus MTR-1105 on the expression of MUC5AC and MUC6 in rat gastric mucosa induced by alcohol in Example 2 is shown in FIG.

[0023] Figure 4The effect of saliva combined with Lactobacillus MTR-1105 on alcohol-induced rat gastric mucosal ZO-1 expression in Example 2 is shown in FIG.

[0024] Figure 5 The effect of saliva combined with Lactobacillus MTR-1105 on the alcohol-induced CAT, MDA, and SOD levels in rat gastric mucosal tissue and plasma in Example 2 (*, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001)

[0025] Figure 6 This is a graph showing the effect of saliva combined with Lactobacillus MTR-1105 on alcohol-induced IL-1β and IL-6 levels in rat gastric mucosal tissue in Example 2 (***, P < 0.001)

[0026] Figure 7 The effect of saliva combined with Lactobacillus MTR-1105 on indomethacin-induced gastric mucosal lesions in rats in Example 3 (**, P<0.01)

[0027] Figure 8 The effect of saliva combined with Lactobacillus MTR-1105 on indomethacin-induced HE and PAS staining of rat gastric mucosa in Example 3 is shown in FIG.

[0028] Figure 9 The effect of saliva combined with Lactobacillus MTR-1105 on the expression of MUC5AC and MUC6 in rat gastric mucosa induced by indomethacin in Example 3 is shown in FIG.

[0029] Figure 10 The effect of saliva combined with Lactobacillus MTR-1105 on indomethacin-induced CAT, MDA, and SOD levels in rat gastric mucosal tissue and plasma in Example 3 (*, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001)

[0030] Specific embodiments of the present invention

[0031] The following will clearly and completely describe the technical solutions in the embodiments of the present invention in conjunction with the accompanying drawings. Obviously, the described embodiments are only some embodiments of the present invention, not all embodiments. Based on the embodiments of the present invention, all other embodiments obtained by ordinary technicians in this field without making creative efforts are within the scope of protection of the present invention.

[0032] In order to make the above-mentioned objects, features and advantages of the present invention more obvious and easy to understand, the present invention is further described in detail below with reference to the accompanying drawings and specific embodiments.

[0033] Example 1 Strain Isolation and Identification

[0034] In a clean environment, fresh healthy human fecal samples were taken, diluted with sterile water, and spread on lactic acid bacteria (MRS) medium and cultured at 37°C for 2-3 days. When significant bacterial colonies were observed, morphologically different colonies were picked and inoculated on freshly prepared MRS medium. The culture was continued at 37°C for 2 days. When monoclonal colonies were observed, monoclonal colonies were picked and further inoculated on freshly prepared MRS medium. The culture was cultured at 37°C for 2 days to obtain purified colonies, numbered MTR-1105. The bacteria were picked and placed in a 20% glycerol aqueous solution and stored at -80°C. At the same time, the collection center was entrusted for identification. Reverse transcription polymerase chain reaction (RT-PCR) was performed using 16S rDNA primers, and 16S rRNA gene sequencing analysis was performed on the isolated strains. Combined with BLAST comparison of the nucleic acid database of the National Center for Bioinformation (NCBI), its species was determined to be Ligilactobacillus salivarius (99.57% homology). The strain of the saliva-associated Lactobacillus MTR-1105 has been deposited in the Guangdong Provincial Microbial Culture Collection Center (deposit number GDMCC 65345, deposit address: No. 100, Xianlie Middle Road, Yuexiu District, Guangzhou City, Guangdong Province).

[0035] Nucleotide sequence of 16S rRNA:

[0036]

[0037] Example 2 Alleviating Effects of Saliva Combined with Lactobacillus MTR-1105 on Alcohol-Induced Gastric Mucosal Lesion in Rats

[0038] 6-8 week old male SD rats were fed adaptively for 1 week and then randomly divided into 5 groups (control group, saliva combined with Lactobacillus MTR-1105 control group, alcohol model group, saliva combined with Lactobacillus MTR-1105 treatment group, and ranitidine treatment group), with 5 rats in each group.

[0039] On days 1 to 14, rats in the saliva combined with Lactobacillus MTR-1105 control group and the saliva combined with Lactobacillus MTR-1105 treatment group were gavaged with saliva combined with Lactobacillus MTR-1105 bacterial solution (5×10 9 CFU / kg, suspended in normal saline); the rats in the ranitidine group were orally administered with ranitidine (20 mg / kg, suspended in normal saline); the rats in the control group and the alcohol model group were orally administered with the same volume of normal saline.

[0040] On day 15, rats in the alcohol model group, the saliva combined with Lactobacillus MTR-1105 treatment group, and the ranitidine treatment group were gavaged with 1 ml of anhydrous ethanol to induce acute gastric mucosal injury. Two hours later, the stomachs of the rats in each group were removed and cut open along the greater curvature to expose the gastric mucosa and photographed. At the same time, the length and width of the bleeding points and bleeding bands were measured with a vernier caliper to calculate the gastric mucosal injury score. The criteria are shown in the table below. Because width represents a much greater severity of injury than length, the width criterion was given double points.

[0041]

[0042] Gastric mucosal injury and scoring results Figure 1 As shown. The results showed that the gastric mucosa of rats in the control group and the saliva combined with Lactobacillus MTR-1105 control group showed normal gastric tissue structure and morphology, with no damage, glossy and smooth surface, and many neatly arranged gastric folds. The gastric mucosa of rats in the alcohol model group was severely damaged, showing a red congestion state and a certain number of ulcers and bleeding spots. The gastric tissue had fewer folds, and the gastric mucus was significantly increased compared with the control group. The gastric mucosa of the saliva combined with Lactobacillus MTR-1105 treatment group and the ranitidine treatment group showed a light pink congestion state and a few ulcers and bleeding spots. The surface of the gastric wall was slightly glossy and the folds were clearer. Compared with the alcohol model group, the degree of gastric mucosal damage in the rats was significantly alleviated.

[0043] The most severely bleeding tissue of the gastric mucosa of the rat was cut out, fixed in 10% formalin solution, stained with hematoxylin-eosin (HE) and periodic acid-Schiff (PAS), and observed under a microscope. Figure 2 As shown, the gastric mucosal structure of rats in the control group and the saliva combined with Lactobacillus MTR-1105 control group was intact, with tightly packed epithelial cells and no bleeding, inflammatory cell infiltration, or submucosal edema. The alcohol-induced model group exhibited significant gastric mucosal pathological changes, with disorganized gastric glands, severe epithelial cell loss, extensive mucosal congestion, inflammatory cell infiltration, and severe submucosal edema. Compared with the alcohol-induced model group, the gastric mucosal damage in the saliva combined with Lactobacillus MTR-1105 and ranitidine-treated groups was relatively mild, with reduced loss and disorder of gastric glandular structure, and improved epithelial cell desquamation and inflammatory cell infiltration. These results indicate that saliva combined with Lactobacillus MTR-1105 inhibits alcohol-induced gastric mucosal pathological changes in rats.

[0044] PAS staining revealed that the gastric mucosal surface of rats in the control group and the saliva combined with Lactobacillus MTR-1105 control group was covered with a complete, uninterrupted purple-red mucus layer. In the alcohol-induced modeling group, rats experienced extensive epithelial cell desquamation, mucosal structural damage, and an incomplete mucus layer could not be observed. The gastric mucosal structure of rats in the saliva combined with Lactobacillus MTR-1105 and ranitidine treatment groups was intact, with increased mucus distribution, similar to the gastric mucosal morphology of rats in the healthy control group. These results suggest that saliva combined with Lactobacillus MTR-1105 inhibits alcohol-induced mucus protein loss in the rat gastric mucosa and improves the mucus barrier function of the gastric mucosa.

[0045] Mucin 5AC (MUC5AC) and mucin 6 (MUC6) are important components of gastric mucin. Immunofluorescence staining of gastric mucosal tissue was further performed to observe the expression of MUC5AC and MUC6 in gastric mucosa. Figure 3 As shown, rats in the control group and the saliva combined with Lactobacillus MTR-1105 control group had more MUC5AC and MUC6-positive cells; the gastric mucosal surface of the model group was damaged, with low expression of MUC5AC and MUC6; the gastric mucosal structure of rats in the saliva combined with Lactobacillus MTR-1105 and ranitidine treatment groups was essentially intact, with significantly increased expression of MUC5AC and MUC6. These results again demonstrate that saliva combined with Lactobacillus MTR-1105 reverses the alcohol-induced decrease in MUC5AC and MUC6 expression, thereby maintaining the integrity of the mucus layer and enhancing mucus barrier function.

[0046] Immunohistochemical staining was further performed on gastric mucosal tissue to observe the expression of tight junction protein ZO-1 in gastric mucosal epithelial barrier. Figure 4 As shown, compared with the control group and the saliva combined with Lactobacillus MTR-1105 control group, the expression of ZO-1 protein in the gastric mucosa of rats in the alcohol modeling group was significantly decreased. ZO-1 expression in the gastric mucosa of rats in the saliva combined with Lactobacillus MTR-1105 treatment group and the ranitidine treatment group was significantly restored. These results indicate that saliva combined with Lactobacillus MTR-1105 upregulates the expression of tight junction-related proteins in the gastric mucosa, maintaining the mechanical barrier function of the gastric mucosa.

[0047] Gastric mucosal tissues of rats in each group were weighed, added with pre-cooled physiological saline, homogenized, and centrifuged for 10 minutes (1000×g, 4°C). The supernatant was collected. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), and catalase (CAT) in the gastric tissues of each group were detected according to the instructions of the superoxide dismutase (SOD) kit, malondialdehyde (MDA), and catalase (CAT) kit. Figure 5As shown, MDA production increased in the gastric mucosal tissue of rats in the alcohol modeling group, while CAT and SOD levels decreased. Compared with the modeling group, MDA levels were significantly reduced and CAT and SOD activities were significantly increased in the gastric mucosal tissue of rats in the saliva combined with Lactobacillus MTR-1105 and ranitidine treatment groups. These results further demonstrate that saliva combined with Lactobacillus MTR-1105 alleviates gastric mucosal damage by reducing oxidative stress.

[0048] The gastric mucosal tissues of rats in each group were weighed, total RNA was extracted, and after reverse transcription, the expression levels of inflammatory factors such as interleukin-1β (IL-1β) and interleukin-6 (IL-6) were determined using real-time fluorescence quantitative PCR (qPCR) technology to evaluate the inflammatory response of the gastric mucosa of rats. Figure 6 As shown, the expression of IL-1β and IL-6 in the gastric mucosal tissue of rats in the alcohol model group was significantly increased. Compared with the model group, the levels of inflammation in the gastric mucosal tissue of rats in the saliva combined with Lactobacillus MTR-1105 and ranitidine treatment groups were significantly reduced. These results suggest that saliva combined with Lactobacillus MTR-1105 inhibits inflammatory responses and alleviates gastric mucosal damage.

[0049] Gastric mucosal tissues of rats in each group were weighed and proteins were extracted. Western blot was used to detect the expression of oxidative stress-related proteins nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1), apoptosis-related proteins B-cell lymphoma 2 (Bcl-2) and cell apoptosis regulator (Bax), and inflammation-related protein cyclooxygenase-2 (COX-2). The results showed that saliva combined with Lactobacillus MTR-1105 colonization improved the alcohol-induced decrease in the expression of Nrf2, HO-1, and Bcl-2 in rat gastric mucosal tissues, and alleviated the alcohol-induced increase in the expression of COX-2 and Bax. This indicates that saliva combined with Lactobacillus MTR-1105 inhibits oxidative stress, inflammation, and apoptosis in gastric mucosal tissues, alleviating gastric mucosal damage.

[0050] Example 3 Alleviating effect of saliva combined with Lactobacillus MTR-1105 on indomethacin-induced gastric mucosal lesions in rats

[0051] 6-8 week old male SD rats were fed adaptively for 1 week and then randomly divided into 4 groups (control group, indomethacin model group, saliva combined with Lactobacillus MTR-1105 treatment group, and ranitidine treatment group), with 5 rats in each group.

[0052] On the 1st to 14th day, the saliva combined with Lactobacillus MTR-1105 treatment group: rats were gavaged with saliva combined with Lactobacillus MTR-1105 bacterial solution (5×10 9CFU / kg, suspended in normal saline); the rats in the ranitidine group were orally administered with ranitidine (20 mg / kg, suspended in normal saline); the rats in the control group and the alcohol model group were orally administered with the same volume of normal saline.

[0053] On the 15th day, rats in the indomethacin model group, the saliva combined with Lactobacillus MTR-1105 treatment group, and the ranitidine treatment group were gavaged with indomethacin (25 mg / kg) to induce acute gastric mucosal injury. Two hours later, the stomachs of rats in each group were taken, cut open along the greater curvature of the stomach, the gastric mucosa was exposed, and photographed. At the same time, a vernier caliper was used to measure the length and width of the bleeding point and the bleeding band, and the gastric mucosal injury score was calculated. The gastric mucosal and pathological scores of rats in each group are as follows: Figure 7 As shown, the gastric mucosa of rats in the indomethacin model group showed red congestion and cord-like hemorrhagic bands, with fewer gastric tissue wrinkles. The gastric mucosa of rats in the saliva combined with Lactobacillus MTR-1105 treatment group and the ranitidine treatment group showed light pink congestion and a small number of hemorrhagic spots. The gastric wall surface was shiny and the wrinkles were clear. The gastric mucosal injury score was significantly reduced, and the degree of gastric mucosal injury was significantly alleviated.

[0054] Cut the most severely bleeding tissue of the rat gastric mucosa, fix it in 10% formalin solution, perform HE staining and PAS staining, and observe under a microscope. Figure 8 As shown, saliva combined with Lactobacillus MTR-1105 and ranitidine treatment significantly reversed indomethacin-induced gastric mucosal pathological changes in rats, restored the number and structural arrangement of gastric glands, and reduced epithelial cell shedding and inflammatory cell infiltration. The results show that saliva combined with Lactobacillus MTR-1105 inhibited alcohol-induced gastric mucosal pathological changes in rats.

[0055] PAS staining revealed that the gastric mucosa of rats treated with saliva combined with Lactobacillus MTR-1105 and ranitidine regained structural integrity, with increased mucus distribution and a relatively continuous purple-red mucus layer covering the gastric mucosal surface. These results suggest that saliva combined with Lactobacillus MTR-1105 inhibited indomethacin-induced mucus protein loss in the rat gastric mucosa and improved the mucus barrier function of the gastric mucosa.

[0056] At the same time, the expression of MUC5AC and MUC6 in gastric mucosal tissue was observed by immunofluorescence staining. Figure 9 As shown, saliva combined with Lactobacillus MTR-1105 and ranitidine significantly reversed the indomethacin-induced decrease in MUC5AC and MUC6 expression in rat gastric mucosal tissue. The results again showed that saliva combined with Lactobacillus MTR-1105 upregulated MUC5AC and MUC6 expression, enhanced mucus barrier function, and alleviated indomethacin-induced gastric mucosal damage in rats.

[0057] The levels of SOD, MDA, and CAT in the gastric tissues of each group were further detected. Figure 10 As shown in the results, compared with the indomethacin-treated group, the saliva combined with Lactobacillus MTR-1105 and ranitidine-treated groups showed a significant decrease in MDA content and a significant increase in CAT and SOD activities in the gastric mucosal tissue. These results further demonstrate that saliva combined with Lactobacillus MTR-1105 alleviates gastric mucosal damage by reducing oxidative stress.

[0058] The above description of the disclosed embodiments is intended to enable one skilled in the art to implement or use the present invention. Various modifications to these embodiments will be readily apparent to one skilled in the art, and the general principles defined herein may be implemented in other embodiments without departing from the spirit or scope of the present invention. Therefore, the present invention is not limited to the embodiments shown herein but is to be construed in the widest possible manner consistent with the principles and novel features disclosed herein.

Claims

1. A human intestinal saliva combined Lactobacillus MTR-1105 strain, deposited in Guangdong Provincial Microbial Culture Collection Center with the accession number GDMCC 65345.

2. A composition, characterized in that The method comprises the strain according to claim 1 or a derivative thereof, wherein the derivative is selected from at least one of live bacteria, inactivated bacteria, freeze-dried bacterial powder, strain metabolites, bacterial lysates or bacterial autolysates.

3. The composition according to claim 2, characterized in that The composition is a functional bacterial agent, preferably a probiotic preparation.

4. The composition according to claim 2, characterized in that: The composition is a functional food and is in a solid, liquid, semi-solid or freeze-dried form.

5. The composition according to claim 4, characterized in that: The functional food includes fermented food prepared by fermenting milk-based, plant-based, grain-based or protein-based raw materials by the strain.

6. The composition according to claim 2, characterized in that: The composition is a medicine, comprising a pharmaceutically acceptable carrier.

7. Use of the composition according to any one of claims 2 to 6 in the preparation of a preparation for preventing or treating acute gastric mucosal damage caused by chemical factors.

8. The use according to claim 7, wherein the damaging factor is selected from alcohol or nonsteroidal anti-inflammatory drugs.

9. The use according to claim 8, wherein the nonsteroidal anti-inflammatory drug is indomethacin.

10. The use according to any one of claims 7 to 9, characterized in that These include alleviating gastric mucosal damage and bleeding, inhibiting excessive inflammatory responses, and reducing oxidative stress levels.

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