TWI718394B - Lactic acid bacteria composition for inhibiting gastritis caused by helicobacter pylori in stomach and its use - Google Patents

Abstract

The present invention provides a pharmaceutical composition and food product for inhibiting gastritis caused by Helicobacter pylori in the stomach, which comprises lactic acid bacteria selected from Lactobacillus rhamnosus GM-020 (also known as GMNL-74), The deposit numbers are BCRC910236 and CCTCC M203098; Lactobacillus acidophilus GMNL-185, the deposit numbers are BCRC910774 and CCTCC M2017764 and Lactobacillus plantarum (Lactobacillus plantarum) GMNL-662, the deposit numbers are BCRC910738 and CCTCC M2016571 and any two The group of the above combination.

Description

Lactic acid bacteria composition for inhibiting gastritis caused by helicobacter pylori in stomach and its use

The present invention relates to the field of health food, and particularly refers to the use of lactic acid bacteria composition to inhibit gastritis caused by Helicobacter pylori in the stomach.

Helicobacter pylori (H.pylori ) is a micro-aerobic gram-negative bacteria that may cause: gastric ulcer, duodenal ulcer, chronic gastritis, gastric mucosa-related Lymphoma (mucosa-associated lymphoid tissue lymphoma), and even gastric adenocarcinoma (gastric adenocarcinoma)... and other gastrointestinal related diseases. Helicobacter pylori mainly uses its urease to decompose urea to produce ammonia and carbon dioxide (CO ₂ ). Ammonia reacts with water to produce alkaline ammonia ions (NH4 ⁺ ) to neutralize gastric acid and increase mucosal acid The alkali value reaches pH 4.5~7.0, which enables bacteria to survive in the stomach environment for a long time (Eaton KA, Suerbaum S, Josenhans C and Krakowka S. 1996) . In addition, Helicobacter pylori secretes vacuolar toxin (vacuolating cytotoxin A, VacA). This cytotoxin will increase cell permeability and cause cell rupture to cause inflammation (Atherton JC, Peek RM, Jr., Tham KT, Cover TL). and Blaser MJ.1997) . Another important toxin is cytotoxin-associated gene A (CagA). Studies have confirmed that CagA can activate nuclear transcription factor κB (NF-κB) to activate downstream inflammation-related cytokine expression; and can promote cells The hormone interleukine-8 (IL-8) is secreted to chemoattract neutrophils (neutrophils) to accumulate, thereby causing downstream inflammation of the gastric epithelium (Backert S, Schwarz T, Miehlke S, Kirsch C, Sommer) C, et al. 2004, Censini S, Lange C, Xiang Z, Crabtree JE, Ghiara P, et al. 1996) , and cause gastrointestinal disorders after Helicobacter pylori infection.

The current treatment of Helicobacter pylori infection usually requires simultaneous administration of the following drugs: (1) Antibiotics, such as: amoxicillin, clarithromycin, metronidazole, etc.; (2) bismuth; (3) acid inhibitor or proton help Pu inhibitor (proton pump inhibitor) and so on. However, Helicobacter pylori is prone to develop resistance to antibiotics, so it is currently combined with three-in-one or four-in-one therapies such as two antibiotics plus bismuth salt or proton pump inhibitor; the main side effects of these drugs are abnormal taste, Obvious side effects such as nausea, diarrhea, flatulence, headache, dizziness, etc., if the patient stops the drug by himself, it is more likely to cause Helicobacter pylori resistance. In general, about 10-20% of patients cannot eradicate Helicobacter pylori infection due to the above reasons. Therefore, there is still room for improvement in existing treatments for Helicobacter pylori infection.

Lactic acid bacteria is confirmed by studies of microorganisms for human health, the most widely used is Lactobacillus (Lactobacillus spp.) And Bifidobacterium (Bifidobacterium spp.). In the adjuvant treatment of Helicobacter pylori infection, in recent years, it has been discovered that the use of specific lactic acid bacteria strains can increase antibiotic therapy , especially when the effects of three-in-one therapy are not effective (Dang Y, Reinhardt JD, Zhou X and Zhang G. 2014) Clearance rate of Helicobacter pylori. In addition, studies have shown that the use of lactic acid bacteria can also reduce the side effects of antibiotic therapy, including nausea, gastrointestinal discomfort and vomiting ( Gong Y, Li Y and Sun Q. 2015, Zhang MM, Qian W, Qin YY, He J and Zhou) YH. 2015, Lv Z, Wang B, Zhou X, Wang F, Xie Y, et al . 2015). Therefore, to find a novel lactic acid bacteria composition to replace antibiotics to treat Helicobacter pylori infection is a problem that the field intends to solve.

In view of this, the inventor deeply understands the shortcomings and shortcomings of the previous proposal, and is eager to improve and innovate, and successfully developed a lactic acid bacteria composition that inhibits Helicobacter pylori in the stomach.

To achieve the above object, the present invention provides a pharmaceutical composition for inhibiting gastritis caused by Helicobacter pylori, which contains lactic acid bacteria selected from Lactobacillus rhamnosus GM-020 (also known as GMNL-74). ), the deposit number is BCRC910236 and CCTCC M203098, Lactobacillus acidophilus (Lactobacillus acidophilus) GMNL-185, the deposit number is BCRC910774 and CCTCC M2017764 and Lactobacillus plantarum (Lactobacillus plantarum) GMNL-662, the deposit number is BCRC910738 and CCTCC M2016571 'S group.

Wherein the pharmaceutical composition is a dosage form for oral administration, and the dosage form is selected from the group consisting of solutions, suspensions, emulsions, powders, lozenges, pills, syrups, lozenges, tablets, chewing gums, thick pastes and capsules. Of the group.

To achieve the above object, the present invention provides another food product, which comprises probiotic Lactobacillus rhamnosus GM-020 (also known as GMNL-74), Lactobacillus acidophilus GMNL-185 and plant Lactobacillus plantarum GMNL-662 and edible materials.

Wherein the edible material is selected from water, fluid milk, concentrated milk, yogurt, yogurt, frozen yogurt, fermented lactobacillus beverage, milk powder, ice cream, cheese, cheese, soy milk, fermented soy milk, vegetable juice, Fruit juice, sports drinks, desserts, jelly, candy, baby food, health food, animal feed, Chinese herbal composition and dietary supplements.

To achieve the above object, the present invention provides another method for preparing a composition for treating gastric Helicobacter pylori infection by lactic acid bacteria, wherein the lactic acid bacteria strain is selected from Lactobacillus rhamnosus GM-020 (also known as Lactobacillus rhamnosus). GMNL-74), Lactobacillus acidophilus GMNL-185 and Lactobacillus plantarum GMNL-662.

Among them, this lactic acid bacteria inhibits the absorption or invasion of gastric cells by Helicobacter pylori, inhibits the interleukin-8 (IL-8) and NF-κB transcription factors induced by gastric Helicobacter pylori, and inhibits the expression of gastric COX-2 protein. Achieve the effect of inhibiting multi-drug resistant Helicobacter pylori and antibiotic-sensitive Helicobacter pylori.

Figure 1 is a sorting diagram of the adsorption capacity of 226 lactic acid strains to human gastric epithelial cells (AGS); Figure 2A is the analysis of IL-8 expression by ELISA; Figure 2B is the analysis of NFκB activity by NF-κB-luminescence enzyme activity; Figure 3A Analysis of lactic acid bacteria inhibiting Helicobacter pylori adsorption on gastric cells; Figure 3B Analysis of lactic acid bacteria inhibiting Helicobacter pylori invading gastric cells; Figure 4A is a flow chart of mice feeding Helicobacter pylori; Figure 4B is a CLO test to analyze the degree of Helicobacter pylori infection in gastric tissue ; Figure 4C is the use of immunohistochemical analysis to analyze the expression of gastric tissue inflammatory protein COX-2.

All technical and scientific terms mentioned in this manual, unless otherwise defined, are meanings that can be understood by the professionals in the field.

The terms "carrier", "vehicle", and "diluent" in this specification refer to non-toxic compounds or agents that have the function of assisting cells or tissues to absorb drugs.

The composition used in the present invention can be further added with an edible material to prepare a food product or health care product. The edible material includes, but is not limited to: water, fluid milk products, milk, concentrated milk; fermented milk, such as yogurt , Sour milk, frozen yoguit, lactic acid bacteria-fermented beverages; milk powder; ice cream; cream cheeses; dry cheeses; soybean milk; fermented soybean milk; vegetable-fruit juices; juices; sports drinks; confectionery; jellies; candy candies; infant formulas; health foods; animal feeds; Chinese herbals; dietary supplements, etc.

The aforementioned composition used in the present invention can be a dietary supplement and can be administered to the user in the following ways: mixed with a suitable drinkable liquid, such as water, yogurt, milk or fruit juice; or can be mixed with solid or liquid food. In this specification, the form of dietary supplement can be lozenge, pill, capsule, lozenge, granule, powder, suspension, sachet, soft lozenge, candy, syrup and corresponding administration form, It is usually in the form of a unit dose and is manufactured in the usual way of preparing dietary supplements.

The lactic acid bacteria used in the present invention is a culture solution of dead bacteria or live bacteria.

The following examples are only examples, and the dosage can be changed according to variations, and is not limited to the activity of the compound used, the treatment of diseases or physiological conditions, the method of administration, individual needs, the severity of the disease, and the judgment of the physician.

Example 1: Screening of lactic acid bacteria that can be highly adsorbed to human gastric cells (AGS)

After co-cultivating human gastric epithelial cells AGS (ATCC CRL 1739) and activated lactic acid bacteria liquid (bacterial infection dose MOI is 100) for 2 hours, the unadsorbed bacteria were washed off with PBS, and stained with Giemsa stain. Use a microscope to observe the number of lactic acid bacteria adsorbed on human gastric epithelial cells (AGS) to evaluate the strength of the strain's adsorption capacity.

Figure 1 shows the observation under the oil microscope field. If there are more than 40 lactic acid strains attached to the cells (as shown in Figure 1A), "++++" indicates that the ability to bind to cells is the strongest; more than 20 lactic acid strains Adsorbed to cells (as shown in Figure 1B), expressed as "+++"; more than 10 lactic acid strains adsorbed on cells (as shown in Fig. 1C), expressed as "++"; more than 3 lactic acid strains adsorbed On the cell (as shown in Figure 1D), it is indicated by "+"; if there is no lactic acid strain attached to the cell (as shown in Figure 1E), it is indicated by "-", which means there is no ability to bind to the cell.

Finally, a total of 226 lactic acid bacteria were analyzed for their ability to bind to human gastric epithelial cells (AGS), and 18 lactic acid bacteria with the strongest binding ability were selected (Figure 1F, marked with "++++") and compared with their ability to withstand gastric acid. Pick out 13 strains of lactic acid bacteria that are more resistant to gastric acid, and then proceed to further screening of strains resistant to gastric Helicobacter pylori.

Example 2: Screening of lactic acid bacteria that can highly inhibit Helicobacter pylori-induced IL-8 secretion and NF-κB transcription factor related inflammation

The gastric epithelial cells infected with Helicobacter pylori were co-cultured with different strains of lactic acid bacteria (13 strains selected in the previous step) for 16 hours, and then the expression level of IL-8 was analyzed by ELISA method, and the NF-κB-luminescence enzyme After the (NF-κB luciferase) construct is colonized into gastric epithelial cells, lactic acid bacteria and Helicobacter pylori are added for co-cultivation for 12 hours, and the NF-κB-luminescence enzyme activity can be analyzed to know the activity of the inflammatory reaction caused by Helicobacter pylori. And further analyze whether the lactic acid bacteria have an inhibitory effect.

The analysis results are shown in Table 1. It can be seen from the table that Lactobacillus rhamnosus GM-020 (also known as GMNL-74, presented as GMNL-74 in the table), Lactobacillus acidophilus The three strains of GMNL-185 and Lactobacillus plantarum GMNL-662 have better ability to inhibit the secretion of IL-8 and the production of NF-κB, and the inhibitory effect is better than that of lactic acid bacteria of the same strain and different strains.

For the three lactic acid bacteria selected from the above table, the deposit number, date and strain name of the lactic acid bacteria are shown in Table 2.

Table 1. Screening results of lactic acid bacteria that inhibit Helicobacter pylori-induced inflammation-related factors

The gastric epithelial cells infected with Helicobacter pylori were co-cultured with lactic acid bacteria containing different strains (13 strains selected in the previous step) for 16 hours, and then the expression level of IL-8 was analyzed by the ELISA method. The results are shown in Table 1 in Figure 2 Three strains were selected for the best inhibition of Helicobacter pylori, among which three strains were statistically significant compared with the experimental group (HP) (*: P <0.01). Figure 2A shows the expression level of IL-8 and carries out statistical analysis. It can be seen from the figure that the three strains can inhibit the immunochemotactic hormone IL-8; Figure 2B shows the relative activity of the NF-κB transcription factor and carries out statistical analysis. It can be seen that the three strains can inhibit the production of the transcription factor NF-κB in the inflammation response pathway. From the above conclusions, it can be seen that the inhibitory strength of the three strains is slightly different, which means that these three strains can inhibit the production of the immunochemotactic hormone IL-8 and the transcription factor NF-κB in the inflammatory response pathway to reduce the infiltration of immune cells into the stomach and Reduce the severity of local inflammatory reactions.

Example 3: The three lactic acid strains screened out simultaneously inhibit Helicobacter pylori Activity of bacteria adhesion and invasion of gastric epithelial cells

To further confirm whether lactic acid bacteria have the ability to inhibit the adhesion activity of Helicobacter pylori to gastric epithelial cells. With lactic acid bacteria, Helicobacter pylori infects human gastric epithelial cells (AGS cells, ATCC CRL1739) with a multiplicity of infection (MOI) dose of 100 (multiplicity of infection, MOI) for 6 hours. After washing the cells, water is used to break the cells, and after serial dilution, they are inoculated into blood culture medium. Count the number of colony-forming units (CFU) after culturing for 3-4 days. The lower the number of CFU, it means that the number of Helicobacter pylori adherent cells is inhibited by lactic acid bacteria.

The gentamicin protection assay was used to analyze the ability of lactic acid bacteria to influence Helicobacter pylori invasion (invasion activity) of gastric epithelial cells. If CFU decreases, it means that lactic acid bacteria have the effect of affecting Helicobacter pylori invading gastric epithelial cells. The infected cells were washed three times with PBS and treated with impermeable gentamicin (100μg/ml) for 1.5 hours to kill the Helicobacter pylori on the surface. After washing, the cells were broken with water, and then inoculated after serial dilution. In the blood culture medium, the number of Helicobacter pylori colonies was counted after 3-4 days of culture.

Figure 3A is an analysis of the ability of Helicobacter pylori to adsorb gastric cells; Figure 3B is an analysis of the ability of Helicobacter pylori to invade gastric cells, in which the ability of simple Helicobacter pylori to adsorb and invade gastric cells is regarded as 100%, and statistical analysis is performed, after comparative analysis Compared with the experimental group (HP), the three strains have statistical significance (*: P <0.01).

The results show that the three strains of lactic acid bacteria can effectively reduce the adsorption of Helicobacter pylori to gastric epithelial cells, and its inhibition can be as high as 90% (as shown in Figure 3A), and can also more effectively reduce the invasion of Helicobacter pylori into epithelial cells, and its inhibition is improved. To more than 99% (as shown in Figure 3B). It means that these three strains have a good effect on inhibiting Helicobacter pylori from adsorbing and invading epithelial cells. In addition, under the two analysis platforms, the inhibition strength of the three strains is slightly different. Therefore, the use of composite strains should be a better strategy.

Example 4. The composition of three lactic acid bacteria has the effect of additively inhibiting antibiotic-sensitive HP or HP strains with multiple drug resistance

The agar-well diffusion method and bacteriostasis test were used to analyze the ability of lactic acid bacteria against Helicobacter pylori strains. The H.pylori disease source strains used include: H.pylori BCRC 26695 (ATCC 700392): wild-type strain, sensitive to the antibiotics metronidazole and clarithromycin; H.pylori v633: resistant to the antibiotic metronidazole ( MZ ^R ) and clarithromycin are resistant (CH ^R ); H.pylori v2311: resistant to the antibiotic metronidazole (MZ ^R ), but sensitive to clarithromycin (CH ^S ). H. pylori was cultured under microaerobic conditions (85% N ₂ , 10% CO ₂ , 5% O ₂ ) and Brucella blood agar plate (BAP) medium. The pathogens were scraped off and the concentration of pathogens was adjusted with PBS 1×10 ⁹ cells/ml, take 100μl of diluted H.pylori and evenly smear it on the quantitative BAP culture plate, let it stand for 15 minutes until the surface of the medium is dry, and use an 11mm diameter glass tube to apply the above-mentioned BAP medium that has been coated with the bacterial solution Dig a hole.

After comparing the antibacterial effect of the whole bacterial liquid and the supernatant liquid from which the bacterial cells were excluded, it was confirmed whether the antibacterial ability of lactic acid bacteria came from the surface material of the bacterial cell or the secreted material of the bacterial cell. The method of collecting the whole bacterial solution is: after GM-020, GMNL-185, and GMNL-662 are activated overnight, they are cultured to MRS broth medium with 1% inoculation amount. After 18 hours of culture, the whole bacterial solution is collected. And at the same time make a mixed whole bacterial solution (the ratio of three strains = 1:1:1); the method of collecting the supernatant of the bacteria is as follows: after GM-020, GMNL-185, and GMNL-662 are activated overnight, use 1 % Inoculation amount was cultured to MRS broth medium. After 18 hours of culture, the whole bacterial solution was collected. After centrifugation at 13000 rpm for 3 minutes, the bacterial cells were removed, and the supernatant was filtered through a 0.45 μm filter membrane, which is the supernatant. Clear liquid, and make a mixed supernatant at the same time (the ratio of three strains = 1:1:1).

Finally, in the antibacterial test, first add 100μl of lactic acid bacteria test sample to the hole, and carefully translate the culture plate in microaerobic conditions and incubate at 37℃. After 48 hours, observe the size of the inhibition zone and use an electronic vernier to measure the inhibition The size of the circle. And statistical analysis by Student's t-test. *, P <0.05 indicates a significant difference to confirm whether the effect of mixed strains is better than that of single strains.

It can be seen from the results that whether it is a gastric Helicobacter pylori strain (HP wild type, antibiotic sensitive) or a gastric Helicobacter pylori strain with single or multiple drug resistance (HP v2311: MZ ^R ; HP v633: MZ ^R , CH ^R ), GM-020 (presented as GMNL-74 in the table), GMNL-185, GMNL-662, the whole bacterial liquid or the supernatant after the bacteria have been eliminated all have obvious antibacterial ability, but the ability to inhibit each pathogen is different (As shown in Table 3 and Table 4); and the antibacterial ability of the whole bacterial liquid is better than that of the supernatant, which means that both the surface substance and the secretion of the bacterial body have the ability to inhibit Helicobacter pylori in the stomach; more particularly GM-020 (presented as GMNL-74 in the table), GMNL-185, and GMNL-662 lactic acid bacteria composition have significantly enhanced antibacterial ability compared with a single strain ( P <0.05), indicating that the use of this lactic acid bacteria composition can enhance the resistance The effect of Helicobacter pylori, and at the same time, the composition can also have a good inhibitory effect against a variety of clinical drug-resistant strains at the same time, and is not subject to the limitations encountered in clinical treatment with antibiotics.

Example 5: The combination of the three lactic acid bacteria can significantly reduce the degree of H. pylori infecting the stomach tissues of mice and reduce the inflammation of the stomach

The Helicobacter pylori mouse test model was used to analyze the inflammatory response of mice to evaluate the protective effect of the lactic acid bacteria composition. The six-week-old BALB/c mice were divided into three groups: the first group was the control group (Mock), the second group was the experimental group (inoculated with Helicobacter pylori), and the third group was the daily tube-fed lactic acid bacteria composition (GM -020+GMNL-185+GMNL-662). The experimental mice in each group were fed water or lactic acid bacteria every day in advance (the third group), and the amount of lactic acid bacteria was 2.4×10 ⁷ CFU/time/mouse until the 24th day. Experimental mice (groups 2 and 3) were inoculated with Helicobacter pylori (as shown in Figure 4A) in the afternoon on the 8th, 10th, 12th, 14th, 16th, and 18th, a total of six times, each with a bacterial count of 1× 10 ⁹ CFU/time/mouse. The Helicobacter pylori inoculation was stopped on the 18th day of feeding, and the lactic acid bacteria continued to be fed.

The mice were sacrificed on the 25th day, the stomach tissues were taken and the CLO (Campylobacter-like Organism Test) was used to analyze the Helicobacter pylori urease activity. If the CLO test medium is red to pink, it means that the mouse stomach is still infected with Helicobacter pylori Bacteria is a positive reaction; if it is yellow, it means a negative reaction. The quantified color depth is drawn as a bar graph (as shown in FIG. 4B), and statistical analysis is performed to analyze whether the lactic acid bacteria composition can inhibit Helicobacter pylori infection. The results of the CLO test are shown in Figure 4B. It was found that the tube fed mixed strain (GM-020+GMNL-185+GMNL-662) group had lower stomach CLO scoring compared with the group only inoculated with Helicobacter pylori. The value is significantly decreased, which is statistically significant compared with the experimental group (HP) (*: P <0.05).

Immunohistochemical staining and background H&E staining were used to analyze the expression of the inflammatory factor cyclooxygenase-2 (COX-2) in gastric tissue, and to evaluate the gastric inflammatory response of lactic acid bacteria against Helicobacter pylori infection to infer the possible mechanism.

The results in Figure 4C show that feeding mixed strains can significantly inhibit COX-2 protein expression.

In summary, the present invention screened 226 strains of lactic acid bacteria, and screened a lactic acid bacteria composition against Helicobacter pylori, including: Lactobacillus rhamnosus GM-020, Lactobacillus acidophilus GMNL -185. Lactobacillus plantarum (Lactobacillus plantarum) GMNL-662, the lactic acid bacteria composition not only has the ability to highly bind to gastric cells, but also reduces the immune chemotaxis and pro-inflammatory response caused by gastric Helicobacter pylori infection; In addition, the lactic acid bacteria composition can effectively inhibit Helicobacter pylori in the stomach from adsorbing and invading gastric cells. Compared with a single strain, the lactic acid bacteria composition has the additive effect of inhibiting multiple Helicobacter pylori strains, indicating that the lactic acid bacteria composition is widely used It is very helpful for the treatment of Helicobacter pylori strains that are clinically resistant to antibiotics.

In addition, both the whole bacterial liquid and the supernatant liquid have the effect of inhibiting Helicobacter pylori strains, and the whole bacterial liquid inhibits Helicobacter pylori better than the supernatant, indicating the surface of GM-020, GMNL-185, GMNL-662 cells Both the substance and the secreted substance of the bacteria have the ability to inhibit Helicobacter pylori in the stomach. Furthermore, the lactic acid bacteria composition can reduce the secretion of the immunochemotactic cytokine IL-8 caused by Helicobacter pylori and the increase of the transcription factor NF-κB related to inflammation, and it can also reduce the gastric COX-2 caused by Helicobacter pylori. This result shows that the lactic acid bacteria composition of this case can be used to prevent or treat the occurrence of subsequent diseases caused by a large number of gastric Helicobacter pylori infections, such as: gastric ulcer, duodenal ulcer, chronic gastritis, gastric cancer, etc., plus The lactic acid bacteria composition in this case is safe and has no side effects, so it can be used as another excellent choice for the treatment of gastric Helicobacter pylori infection-related diseases.

The above-mentioned embodiments are only to illustrate the technical ideas and features of the present invention, and their purpose is to enable those who are familiar with this technique to understand the content of the present invention and implement them accordingly. When they cannot be used to limit the scope of the present invention, that is, All equal changes or modifications made in accordance with the spirit of the present invention should still be covered by the patent scope of the present invention.

【Biological Material Deposit】 Domestic deposit information [please note in the order of deposit institution, date and number]

4. Biological Resources Conservation and Research Center of Hsinchu Food Industry Development Research Institute, the deposit date is November 18, 2003, and the deposit number is BCRC 910236.

5. Biological Resources Conservation and Research Center of Hsinchu Food Industry Development Institute, the deposit date is August 12, 2016, and the deposit number is BCRC 910738.

6. Biological Resources Conservation and Research Center of Hsinchu Food Industry Development Research Institute, the deposit date is April 14, 2017, and the deposit number is BCRC 910774.

Foreign hosting information [please note in the order of hosting country, institution, date and number]

1. China, China Type Culture Collection, the deposit date is December 18, 2003, and the deposit number is CCTCC M 203098.

2. China, China Type Culture Collection, the deposit date is October 17, 2016, and the deposit number is CCTCC M 2016571.

3. China, China Type Culture Collection, the deposit date is November 3, 2017, and the deposit number is CCTCC M 2017764.

Claims (6)

A Lactobacillus acidophilus GMNL-185 for inhibiting gastritis caused by Helicobacter pylori in the stomach, its deposit number is BCRC910774 and CCTCC M2017764; wherein the Helicobacter pylori in the stomach is a multi-drug resistant Helicobacter pylori strain or antibiotic sensitive Helicobacter pylori strain, the drug resistance is resistance to the antibiotics metronidazole and clarithromycin. Use of a lactic acid bacteria for preparing a pharmaceutical composition for treating gastric Helicobacter pylori infection, wherein the lactic acid bacteria comprises Lactobacillus rhamnosus GM-020 (also known as GMNL-74), Lactobacillus acidophilus ) GMNL-185 and Lactobacillus plantarum GMNL-662; the deposit numbers of Lactobacillus rhamnosus are BCRC910236 and CCTCC M203098, the deposit numbers of Lactobacillus acidophilus are BCRC910774 and CCTCC M2017764, the Lactobacillus plantarum is deposited The number is BCRC910738 and CCTCC M2016571; wherein the gastric Helicobacter pylori is a multi-drug resistant Helicobacter pylori strain or an antibiotic-sensitive Helicobacter pylori strain, and the drug resistance is resistant to the antibiotics metronidazole and clarithromycin; wherein the lactic acid bacteria system inhibits the stomach Helicobacter pylori adsorbs or invades gastric cells to achieve the effect of inhibiting gastric Helicobacter pylori. The use as described in item 2 of the scope of patent application, wherein the lactic acid bacteria can further inhibit the interleukin-8 (IL-8) and NF-κB transcription factors induced by gastric Helicobacter pylori. The use described in item 2 of the scope of patent application, wherein the lactic acid bacteria can further inhibit the expression of COX-2 protein in the stomach. The use as described in item 2 of the scope of patent application, wherein the lactic acid bacteria refers to a culture medium containing one or all of the surface material of the bacteria or the secretion of the bacteria. The use described in item 2 of the scope of patent application, wherein the lactic acid bacteria are live bacteria.

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