A polypeptide and its application in the treatment of gastric ulcers

Abstract

This invention provides a polypeptide and its application in the treatment of gastric ulcers. Specifically, the present invention isolates and prepares the polypeptide GU-C from sea buckthorn. This polypeptide can effectively promote the proliferation of human gastric mucosal epithelial cells GES-1 and significantly reduce the expression of bFGF. In mouse experiments, this polypeptide can reduce the ulcer index and increase the ulcer inhibition rate in mice with stress-induced gastric mucosal injury, showing a certain dose-response relationship, and has good application prospects.

Description

Technical Field

[0001] This application relates to the field of biology, specifically to a polypeptide and its application in the treatment of gastric ulcers. Background Technology

[0002] Gastric ulcer is a common and frequently occurring clinical disease. Its occurrence is mainly related to an imbalance between invasive factors of mucosal damage and the body's own defense and repair factors. Helicobacter pylori infection, nonsteroidal anti-inflammatory drugs (NSAIDs), and abnormal gastric acid secretion are common causes. Drugs, stress, and hormones can lead to ulcers, while psychological factors and unhealthy lifestyle habits can also induce them. Typical gastric ulcer pain is characterized by its long-term, periodic, and rhythmic nature. With the accelerated pace of life, unhealthy lifestyle habits, and increased social, work, family, and psychological burdens, the incidence of gastric ulcers has been increasing year by year. The onset of gastric ulcers shows a clear seasonality, generally occurring more frequently in cold seasons and seasons with large temperature fluctuations. The incidence is lowest in summer when the climate is stable. Age is significantly correlated with the incidence of gastric ulcers; the older the age, the higher the incidence, with 50-60 years old being the peak age range. It is more common in men, with a male-to-female ratio of 3.6:1. The recurrence rate is 60%–80%, and approximately 10% of people will experience it at some point in their lives. The incidence rate varies significantly among different countries. Different periods, geography, climate, ethnicity, genetics and lifestyle all have a certain influence on the epidemiology of gastric ulcers.

[0003] Gastric ulcers, a common digestive tract disease, still lack a unified understanding in modern medicine regarding their pathogenesis and mechanisms. Currently, modern medical understanding of gastric ulcers mainly focuses on theories such as trauma, balance, vascularity, bacterial infection, inflammation, and digestion. The most widely accepted pathogenesis of gastric ulcers is the "balance theory," which states that ulcer formation results from an imbalance between aggressive and defensive factors. Aggressive factors primarily include gastric acid, pepsin, and Helicobacter pylori infection, while defensive factors mainly include gastric mucosal blood flow and the gastric mucosal barrier function. An imbalance in these defensive factors leads to the development of gastric ulcers. Therefore, modern medical treatment for gastric ulcers primarily focuses on inhibiting gastric acid secretion and protecting the gastric mucosa. Gastric mucosal protectants are drugs that protect and enhance the defensive function of the gastric mucosa. They not only protect the gastrointestinal mucosal barrier but also have cytoprotective effects. Gastric mucosal protectants, once inside the gastrointestinal tract, can rapidly bind to the mucosa, forming a thin film that covers the mucosal surface and protects it from various harmful substances. Commonly used gastric mucosal protectants in clinical practice include colloidal bismuth, sucralfate, and methylphenidate.

[0004] In clinical practice, gastric ulcers are mostly treated with medication, and to prevent recurrence, acid-suppressing drugs are usually used for maintenance. Drugs for treating gastric ulcers can be broadly divided into two categories: those that weaken the attacking factor (the digestive action of gastric acid), represented by acid suppressants, and those that enhance mucosal protection factors, represented by bismuth potassium citrate. Proton pump inhibitors, represented by omerazole, have a strong inhibitory effect on gastric acid secretion and few side effects. Their chemical structure consists of a benzimidazole ring, a pyridine ring, and a sulfinyl group connecting these two ring systems. The irreversible inhibition of gastric acid secretion caused by the binding of the sulfinyl group to H+ / K+-ATPase may lead to hypergastrinemia and gastric cancer. While research is being conducted to improve these inhibitors, reversible proton pump inhibitors without the sulfinyl group are also being developed. Reversible proton pump inhibitors inhibit H+ / K+-ATPase activity by competitively binding to K+, and are also known as potassium-competitive acid blockers (P-CABs) or acid pump blockers. These drugs inhibit H+ / K+-ATPase through ionotropic binding, and their activity is restored upon dissociation. They can be classified into imidazopyridine, phthaloylsulfadiazine, isimidazole, and quinoline derivatives. Some formulations have entered Phase II (AZD0865) and Phase III (revaprazan) clinical trials. Revaprazan's trials showed that its acid-suppressing effect is four times that of omeprazole, and the reversible competitive inhibition of P-CABs does not pose a risk of gastric cancer, potentially making it a next-generation acid-suppressing drug.

[0005] Natural drug treatment for gastric ulcers is also an important research direction. Artemisinin and water extracts of *Gentiana scabra* have been extracted from *Gentiana scabra* and have shown significant effects on gastric ulcers in rats with pyloric ligation. Furthermore, the water extract of *Gentiana scabra* also exhibits anti-stress ulcer activity. Xia Ming et al.'s study on the anti-gastric ulcer activity of *Melia azedarach* extract in mice showed that the extract can protect gastric mucosal epithelial cells and inhibit ulcer formation. *Melia azedarach* is a non-toxic vegetable, demonstrating its superiority in preventing and treating gastric ulcers. Ethyl acetate extracts of *Cephalotaxus fortunei* root and ethyl acetate extracts of *Honeysuckle chinensis* have both been shown to have strong anti-ulcer activity. The mechanisms of action of most natural active ingredients involve scavenging free radicals, increasing NO levels, and increasing the content of prostaglandins (PGE) in the mucosa, thereby enhancing mucosal resistance and promoting mucosal repair. *Salvia miltiorrhiza* can enhance the expression of basic fibroblast growth factor (bFGF), thereby promoting ulcer healing. Research on single-herb Chinese medicines mainly focuses on their pharmacological effects on digestive tract ulcers. Studies of 53 commonly used traditional Chinese medicines for treating stomach ailments have shown that Coptis chinensis (berberine), rhubarb, cinnamon twig, dried plum, Corydalis yanhusuo, Panax notoginseng, Magnolia officinalis, and Codonopsis pilosula have strong inhibitory effects on Helicobacter pylori (Hp). Dandelion, Hedyotis diffusa, Scutellaria barbata, Cynanchum paniculatum, Euphorbia humifusa, Curcuma zedoaria, and Scutellaria baicalensis all have the ability to kill Hp. Their active substances have also been largely elucidated. The effects of traditional Chinese medicine in promoting healing, inhibiting bacteria, and preventing recurrence have been affirmed. Especially in killing Hp, traditional Chinese medicine has fewer side effects and is therefore superior to chemical drugs.

[0006] Although there are already many drugs available for treating gastric ulcers, further development is needed to find drugs that are more effective, inexpensive, and readily available. Summary of the Invention

[0007] Studies have shown that peptides and sterols in sea buckthorn are beneficial. Sea buckthorn is a traditional Chinese medicine, and its fruit contains peptides (such as sea buckthorn polysaccharide peptides) that have a protective effect on the gastric mucosa. Peptides can promote the proliferation of gastric mucosal cells and accelerate damage repair. Based on existing research findings, the inventors specifically extracted peptides with good therapeutic effects from sea buckthorn fruit to improve the therapeutic effect.

[0008] On the one hand, the polypeptide for treating gastric ulcers provided by the present invention is named GU-C, and its amino acid sequence is shown in SEQ ID NO: 1.

[0009] In another aspect, the present invention provides a medicament for treating gastric ulcers, characterized in that it contains a polypeptide GU-C for treating gastric ulcers, the amino acid sequence of which is shown in SEQ ID NO: 1.

[0010] Furthermore, the drug also contains a pharmaceutically acceptable carrier or excipient.

[0011] Furthermore, the pharmaceutical excipients of the present invention may be selected from conventional excipients, such as, but not limited to, solubilizers, binders, fillers, disintegrants, lubricants, pH adjusters, penetration enhancers, release regulators, preservatives, coating agents, carriers, flavor masking agents, and combinations thereof.

[0012] When present in solid dosage forms, these may include, but are not limited to, granules, pills, tablets, capsules, powders, films, lozenges, compressible tablets, soluble tablets, disintegrating tablets, dispersible tablets, film-coated tablets, and any of the aforementioned solid forms in a controlled, sustained, prolonged, or delayed-release form. Such formulations may also be in the form of immediate-release, delayed-release, or delayed-release formulations. Furthermore, immediately-release compositions may be conventional, dispersible, chewable, orally soluble, or fast-dissolving formulations, while delayed-release compositions may contain hydrophilic or hydrophobic, or a combination of hydrophilic and hydrophobic, release-rate-controlled substances to form a matrix or reservoir, or a combination of a matrix and reservoir system.

[0013] To prepare the pharmaceutical compositions of the present invention, the active ingredient of the present invention can be mixed with pharmaceutically acceptable carriers, adjuvants, and / or excipients according to conventional pharmaceutical formulation techniques. Pharmaceutically acceptable carriers that can be used in the compositions of the present invention include any standard pharmaceutical carrier, such as phosphate-buffered saline solutions, water, and emulsions, such as oil / water or water / oil emulsions, as well as various types of wetting agents. The compositions may also contain solid pharmaceutical excipients, such as starch, cellulose, talc, glucose, lactose, sucrose, gelatin, malt, rice, flour, chalk, silica gel, magnesium stearate, sodium stearate, glyceryl monostearate, sodium chloride, skim milk powder, etc. Liquid and semi-solid excipients can be selected from glycerol, propylene glycol, polyethylene glycol, water, ethanol, and various oils, including petroleum, animal, plant, or synthetic oils, such as peanut oil, soybean oil, mineral oil, sesame oil, etc. Liquid carriers, particularly liquid carriers for injectable solutions, include water, saline, glucose aqueous solutions, and ethylene glycol.

[0014] Examples of suitable pharmaceutically acceptable wetting agents or surfactants include, but are not limited to, amphoteric, nonionic, cationic, or anionic molecules. Suitable surfactants include, but are not limited to, polysorbates, sodium lauryl sulfate, dodecyl dimethylamine oxide, sodium docusate, hexadecyl trimethylammonium bromide (CTAB), polyethoxylated alcohols, polyoxyethylene dehydrated sorbitol, octylbenzeneol, N,N-dimethyldodecylamine-N-oxide, hexadecyl trimethylammonium bromide, polyoxyethylene (10) lauryl ether, surfactants (vegetable oil-based fatty alcohol polyoxyethylene ethers derived from lauryl alcohol, cetyl alcohol, stearyl alcohol, and oleyl alcohol), bile salts (e.g., sodium deoxycholate and sodium cholate), polyoxyethylene castor oil, nonylphenol ethoxylate, cyclodextrin, lecithin, mebenzyl chloride, carboxylates, sulfonates, petroleum Sulfonates, alkylbenzene sulfonates, naphthalene sulfonates, olefin sulfonates, alkyl sulfates, sulfates, sulfated natural oils and fats, sulfated esters, sulfated alkanolamides, alkylphenols (ethoxylated and sulfated), ethoxylated fatty alcohols, polyoxyethylene surfactants, carboxylic acid esters, polyethylene glycol esters, sorbitan esters and their ethoxylated derivatives, fatty acid glycol esters, carboxamides, monoalkanolamine condensates, polyoxyethylene fatty acid amides, quaternary ammonium salts, amines with amide bonds, polyoxyethylene alkylamines and polyoxyethylene alicyclic amines, N,N,N,N-tetrasubstituted ethylenediamine, 2-alkyl-1-hydroxyethyl-2-imidazoline, N-coco-3-aminopropionic acid / sodium salt (N-coco The surfactants include 3-aminopropionic acid / sodium salt, N-tallow 3-iminodipropionate disodium salt, N-carboxymethyl-N,N-dimethyl-N-9-octadecenyl ammonium hydroxide, N-cocamidoethyl-N-hydroxyethylglycinate sodium salt, polyoxyethylene, sorbitan monolaurate and stearate, (polyethoxylated castor oil), (ethylene oxide / 12-hydroxystearic acid), polysorbate, tetrabutylphenol, and any combination thereof. Preferred pharmaceutically acceptable surfactants include tetrabutylphenol and (sorbitan monooleate) or mixtures thereof.

[0015] The appropriate dosage according to the invention and as described herein in various embodiments can vary depending on the condition, age, and species of the subject, and can be readily determined by those skilled in the art. The total daily dose used in veterinary and human medicine will suitably be in the range of 0.01-2000 mg / kg body weight, preferably 0.1-1000 mg / kg body weight, more preferably 1-100 mg / kg body weight, and these can be administered as a single dose or in divided doses, and may exceed the upper limit when indicated. This dosage can be adjusted according to individual requirements in each case, including the specific peptide administered, the route of administration, the disease being treated, and the patient being treated. However, these peptides can also be administered weekly, monthly, or even at longer intervals as long-acting formulations (implants, sustained-release formulations, etc.). In this case, the dose can be much higher than the daily dose and can be adjusted according to the form of administration, body weight, and specific indication. A suitable dosage can be determined by conducting routine model testing, preferably in animal models. Generally, for oral or parenteral administration to an adult weighing about 70 kg, a daily dose of about 10 mg to about 10,000 mg, preferably about 200 mg to about 1,000 mg, should be appropriate, although the upper limit may be exceeded when indicated. It should be understood that the above-mentioned therapeutically effective dose is not necessarily the result of a single dose, but usually the result of multiple unit doses. Those unit doses may include portions of a daily or weekly dose; therefore, the therapeutically effective dose is determined during treatment (exposure). For example, for oral administration, the daily dose may be about 0.04 to about 1.0 mg / kg body weight, more preferably about 0.04 to about 0.20 mg / kg / day, even more preferably about 0.05 to about 0.15 mg / kg / day, and most preferably about 0.1 mg / kg body weight. Generally, the dosage of the active substance can vary within a relatively wide range to achieve and preferably maintain the desired plasma concentration. Unit dosage forms of the active ingredient may contain about 0.1 mg to about 15 mg of the active ingredient. Preferred unit dosage forms contain about 0.1 to about 1 mg of the drug and can be administered 2 to 5 times daily. However, it should be noted that other alternative routes have also been considered, such as continuous infusion at rates designed to maintain the aforementioned plasma concentrations. The duration of a particular treatment may also vary depending on the severity of the disease, whether the treatment is for acute presentation or prophylaxis, and similar considerations. Typical administration lasts approximately 5 to approximately 14 days, usually a 7-day course.

[0016] Beneficial effects

[0017] This invention provides a polypeptide and its application in the treatment of gastric ulcers. Specifically, the present invention isolates and prepares the polypeptide GU-C from sea buckthorn. This polypeptide can effectively promote the proliferation of human gastric mucosal epithelial cells GES-1 and significantly reduce the expression of bFGF. In mouse experiments, this polypeptide can reduce the ulcer index and increase the ulcer inhibition rate in mice with stress-induced gastric mucosal injury, showing a certain dose-response relationship, and has good application prospects. Attached Figure Description

[0018] Figure 1 Results of the effect of peptides on the proliferative activity of human gastric mucosal epithelial cells GES-1. The groups correspond to the normal group, model group, positive control omeprazole group, low-dose peptide GU-C group, and high-dose peptide GU-C group, respectively.

[0019] Figure 2 The effect of peptides on the ulcer index of gastric ulcers in mice, with corresponding groups: normal group, model group, positive control omeprazole group, low-dose peptide GU-C group, and high-dose peptide GU-C group. Detailed Implementation

[0020] Those skilled in the art can refer to the content of this document and appropriately improve the process parameters to achieve the desired results. It should be particularly noted that all similar substitutions and modifications are obvious to those skilled in the art and are considered to be included in this invention. The methods and applications of this invention have been described through preferred embodiments. Those skilled in the art can obviously modify or appropriately change and combine the methods and applications described herein without departing from the content, spirit, and scope of this invention to implement and apply the technology of this invention. Unless otherwise specified, the methods, equipment, and materials in the following embodiments are all conventional methods, equipment, and materials in the art and are commercially available.

[0021] Example 1: Preparation and Screening of Seabuckthorn Fruit Polypeptides

[0022] The pulp of the sea buckthorn fruit was removed, and the seeds were collected. After washing with clean water, the seeds were crushed, sieved, and impurities were removed. Ultrapure water was added at a material-to-liquid ratio of 1:20 (m / V) and soaked overnight. The supernatant was collected by centrifugation to obtain a crude extract of sea buckthorn seed protein. Bromelain and papain were added to the crude extract for enzymatic hydrolysis for 3 hours each, with an enzyme dosage of 3000 U / g (sea buckthorn seed powder), pH 7, and hydrolysis temperature of 55 degrees Celsius. After enzyme inactivation and centrifugation, the supernatant was collected and ultrafiltered using ultrafiltration membranes with different retention cutoffs. The fraction with a molecular weight less than 3 kDa that showed the best effect on promoting the proliferation of human gastric mucosal epithelial cells was further separated by Sephadex G-25 gel chromatography. Fraction No. 3 showed the best effect on promoting the proliferation of human gastric mucosal epithelial cells and was further separated and purified by HPLC. Fraction I was identified as having the highest activity. The amino acid sequence of the polypeptide GU-C was determined by mass spectrometry and is shown in SEQ ID NO: 1. Sequence 1 was further synthesized artificially for later use.

[0023] Example 2: Cell viability identification of peptide GU-C

[0024] Human gastric mucosal epithelial cells GES-1 (EK-Bioscience, catalog number CB-Y1572) were cultured in DMEM high-glucose medium containing 100 mL / L fetal bovine serum in a standard CO2 incubator for 2-3 days, and passaged when approximately 90% of the cells reached full capacity. The gastric mucosal epithelial cells were then treated with a culture medium containing 7% ethanol for 3 hours, resulting in a 40% inhibition rate and creating a gastric mucosal epithelial cell damage model.

[0025] The experimental cells were divided into: normal group, model group, positive control omeprazole group, low-dose GU-C peptide group, and high-dose GU-C peptide group. The specific experimental steps are as follows: Logarithmic growth phase cells were collected, and the cell density was adjusted to 5 × 10⁻⁶ cells / year. 3At a rate of 100 μL per well, GES-1 cells were seeded into 96-well plates and cultured at 37°C with 5% CO2 for 24 hours. After cell adhesion, the culture supernatant was aspirated, and the cells were washed three times with PBS. Normal GES-1 cells were added to complete culture medium, while the remaining cells were incubated with the selected concentration of ethanol for a certain period. The culture supernatant was then aspirated, and the cells were washed three times with PBS. Each experimental group of GES-1 cells was then added to 100 μL of culture medium containing the corresponding drug at different concentrations. The normal and model groups were not added to the drug, and the cells were cultured for another 24 hours. Specifically, the drug concentration in the positive control omeprazole group was 200 μg / mL, the drug concentration in the low-dose GU-C group was 50 μg / mL, and the drug concentration in the high-dose GU-C group was 200 μg / mL. Each group had five replicates. After 24 hours of culture, 10 μL of 5% MTT was added, and the cells were cultured for another 4 hours. The culture medium was carefully aspirated, and 100 μL of DMSO was added to each well, and the cells were dissolved by shaking at room temperature for 10 minutes. The absorbance (OD) value was measured using a microplate reader at a wavelength of 490 nm, and cell viability was calculated using the MTT assay. Results are as follows: Figure 1 As shown.

[0026] from Figure 1 It can be seen that the OD value of the model group was significantly lower than that of the normal group (P<0.01), while the OD values ​​of all treatment groups were significantly increased after treatment. In particular, the OD value of the high-dose peptide GU-C group reached (1.114±0.050), which was significantly higher than the OD value of the positive control group and also significantly higher than the OD value of the model group.

[0027] After collecting the cell supernatant from each group, the cells were washed three times with PBS, the PBS was discarded, and the cells were digested with trypsin and collected. Cell lysis buffer was added, and the cells were centrifuged at 10,000 rpm for 30 min at 4°C. The supernatant, which was the total cellular protein, was collected and subjected to SDS-PAGE gel electrophoresis. After electrophoresis, the proteins were transferred to a nitrocellulose membrane using electrotransfer. The primary antibody was bFGF antibody, the secondary antibody was goat anti-rabbit horseradish peroxidase antibody, and β-actin protein was used as a control. The colorimetric reaction was performed using ECL chemiluminescence. The detection results were captured on X-ray film. The scanned images were saved as computer files, and the western blot bands were scanned using ImageJ imaging software. The ratio of the gray value of the bFGF protein band to the gray value of the internal control β-actin was used as the relative expression level of the protein. The results are shown in Table 1.

[0028] Table 1. Results of relative expression levels of bFGF protein in each group

[0029] Group bFGF / β-actin ratio normal group 0.241±0.023 Model group 1.096±0.037# Positive control omeprazole group 1.542±0.048# Low-dose group of peptide GU-C 0.953±0.028# High-dose group of peptide GU-C 0.849±0.014#

[0030] As shown in Table 1, the expression of bFGF in the model group was significantly higher than that in normal gastric mucosal cells. The peptide of the present invention can significantly reduce the expression of bFGF with increasing dosage, but there is still a certain gap compared with the normal group. This may be related to the fact that the cells are in the scar stage, but it has been able to significantly reduce bFGF and has a good therapeutic effect.

[0031] Example 3: Animal experiments with peptide GU-C

[0032] ICR clean-grade male mice, weighing 18–22 g, were provided by Beijing Vital River Laboratory Animal Technology Co., Ltd. They were housed at a temperature of 18–25℃ and a relative humidity of 55%–60%. They were randomly divided into 5 groups (n=10 per group) according to body weight: normal group, model group, high- and low-dose GU-C polypeptide groups, and positive control group. The normal and model groups were administered distilled water by gavage at 25 mL / (kg·d); the high- and low-dose polypeptide groups were administered high- and low-concentration GU-C polypeptide solutions by gavage at 25 mL / (kg·d), with drug concentrations of 200 and 50 μg / mL, respectively; the positive control group was administered omeprazole by gavage at 25 mL / (kg·d), with a drug concentration of 200 μg / mL, for 10 consecutive days, once daily. After the last administration, mice were fasted for 12 hours, but water was allowed. Mice were placed in specially designed cages and immersed in water at (18±1)℃, with the water level maintained at the xiphoid process of the sternum. After 20 hours of water stress, they were removed and dried. Blood was collected by enucleation of the eyeballs; mice were euthanized by cervical dislocation, and the abdomen was dissected to collect the liver; the pylorus was ligated, and 1.5 mL of 0.4 g / 100 mL formalin solution was administered by gavage. The cardia was then ligated, the stomach was freed, and fixed for 30 minutes. The stomach was then cut along the greater curvature, and the contents were flushed out with 0.9 g / 100 mL sodium chloride solution and flattened. Microscopic examination of the gastric mucosa was used as an indicator of ulceration.

[0033] The ulcer index and ulcer inhibition rate of mice in each group were calculated according to the Guth criteria, and scores were given based on the area of ​​ulcers or erosions. For pinpoint bleeding: 1 point was awarded for every 3 pinpoint ulcers (mucosal defects less than 1 mm or small hemorrhagic erosions). For linear bleeding: the ulcer index was calculated by measuring the maximum long axis and the maximum wide axis perpendicular to the maximum long axis using calipers. 1 point was awarded for each millimeter of ulcer width; 2 points for each millimeter of ulcer width; and 3 points for each millimeter of ulcer width.

[0034] A / %=

(I1-I2) / I1

[0035] In the formula: A represents the ulcer inhibition rate (%); I1 represents the average ulcer index of the model control group; I2 represents the average ulcer index of the drug-treated group. The results are as follows: Figure 2 As shown.

[0036] from Figure 2It can be seen that the ulcer index in the model group was significantly higher than that in the normal group (P<0.01), while the ulcer index in the positive control group and the polypeptide treatment group decreased significantly after treatment. This indicates that all three treatment groups can significantly reduce the ulcer index, especially the high-dose group, where the ulcer index was only (5.18±0.81)%, showing excellent therapeutic effect. This also demonstrates that GU-C polypeptide can reduce the ulcer index and improve the ulcer inhibition rate in mice with stress-induced gastric mucosal injury, exhibiting a certain dose-response relationship.

[0037] Furthermore, the MDA content and SOD activity of gastric mucosal tissue were detected. Specifically, 200 mg of gastric mucosal tissue was extracted from the ulcer site, weighed, and homogenized with double-distilled water at a ratio of 1:20 to prepare a 5 g / 100 mL tissue homogenate. The homogenate was stored at -20℃ for later use. The MDA content and SOD activity were detected according to the kit instructions. The results are shown in Table 2.

[0038] Table 2. Effects of GU-C peptide on SOD and MDA content in gastric mucosa of model mice.

[0039] Group MDA content (nmol / mgpro) SOD content (nmol / mgpro) normal group 34.91±0.87 21.56±1.45 Model group 92.75±2.08# 8.78±0.96# Positive control omeprazole group 53.87±1.34#* 11.18±1.10# Low-dose group of peptide GU-C 49.71±0.76#* 15.79±1.37* High-dose group of peptide GU-C 42.16±0.41#* 19.17±1.52*

[0040] As shown in Table 2, GU-C peptides significantly increased SOD content and decreased MDA content in the gastric mucosa of model mice, exhibiting a dose-dependent effect; the effect increased with increasing peptide concentration. This indicates that GU-C peptides can also increase the level of free radical scavenging enzymes in the gastric mucosa and slow down lipid peroxidation, thereby playing a role in the treatment of gastric ulcers.

[0041] Although embodiments of the present invention have been described above in conjunction with the accompanying drawings, the present invention is not limited to the specific embodiments and application fields described above. The specific embodiments described above are merely illustrative and instructive, and not restrictive. Those skilled in the art can make many other forms based on the guidance of this specification and without departing from the scope of protection of the claims of the present invention, and all of these are within the scope of protection of the present invention.

Claims

1. A polypeptide GU-C for treating gastric ulcers, characterized in that... The amino acid sequence is shown in SEQ ID NO:

1.

2. A drug for treating gastric ulcers, characterized in that... The invention contains a polypeptide GU-C for treating gastric ulcers, the amino acid sequence of which is shown in SEQ ID NO:

1.

3. Use of polypeptide GU-C in the preparation of a medicament for treating gastric ulcers, wherein the amino acid sequence of the polypeptide is shown in SEQ ID NO:

1.

4. The use as described in claim 3, characterized in that... The drug also contains a pharmaceutically acceptable carrier.

5. The use as described in claim 4, characterized in that... The pharmaceutically acceptable carriers include excipients.

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