CN110628660B - Lactobacillus composition for inhibiting gastritis caused by gastric helicobacter pylori and application thereof - Google Patents

Lactobacillus composition for inhibiting gastritis caused by gastric helicobacter pylori and application thereof Download PDF

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CN110628660B
CN110628660B CN201810666262.XA CN201810666262A CN110628660B CN 110628660 B CN110628660 B CN 110628660B CN 201810666262 A CN201810666262 A CN 201810666262A CN 110628660 B CN110628660 B CN 110628660B
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陈奕兴
蔡宛桦
陈雅惠
赖志河
林宥欣
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Genmont Biotechnology China Co ltd
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Abstract

The invention relates to the field of health-care food, in particular to a lactobacillus composition for inhibiting gastritis caused by helicobacter pylori and application thereof. The invention provides a pharmaceutical composition and a food product for inhibiting gastritis caused by gastric helicobacter pylori, which comprises Lactobacillus selected from GM-020 (also called GMNL-74) of Lactobacillus rhamnosus, with the registration number of CCTCC NO: M203098; lactobacillus acidophilus (Lactobacillus acidophilus) GMNL-185 with accession number of CCTCC NO: M2017764 and Lactobacillus plantarum (Lactobacillus plantarum) GMNL-662 with accession number of CCTCC NO: M2016571 and any two or more combinations thereof.

Description

Lactobacillus composition for inhibiting gastritis caused by gastric helicobacter pylori and application thereof
Technical Field
The invention relates to the field of health-care food, in particular to application of a lactobacillus composition in preparing a composition for inhibiting gastritis caused by helicobacter pylori.
Background
Helicobacter pylori (h. pylori) is a microaerophilic gram-negative bacterium that may be caused to contain: gastrointestinal related diseases such as gastric ulcer (gastroduodenal), duodenal ulcer (duodenal ulcer), chronic gastritis (chronic gastritis), gastric mucosa-associated lymphoma (muco-associated lymphoma), and gastric adenocarcinoma (gastroduodenal) …. Helicobacter pylori mainly utilizes urease (urea) to decompose urea to produce ammonia (ammonia) and carbon dioxide (CO)2) The reaction of ammonia with water produces basic ammonium ions (NH 4)+) The gastric acid is neutralized, the pH value of the mucous membrane is increased to 4.5-7.0, and the bacteria can survive in the stomach environment for a long time (Eaton KA, Suerbaum S, Josenhans C and Krakowka S.1996). In addition, H.pylori secretes vacuolar toxin (VacA), which increases cell permeability and causes cell bursting to cause an inflammatory response (Atherton JC, Peek RM, Jr., Tham KT, Cover TL and blast MJ.1997). The other important toxin is cytotoxin-associated gene A (CagA), and research proves that the CagA can activate nuclear transcription factor kappa B (NF-kappa B) to activate the expression of downstream inflammation-associated cytokines; and can promote secretion of cytokine mediated protein-8 (IL-8) to chemotact aggregation of neutrophils (neutrophiles), thereby causing downstream inflammatory response of gastric epithelium (Backert S, Schwarz T, Miehlke S, Kirsch C, Sommer C, et al.2004, cennsin S, Lange C, Xiang Z, Crabtree JE, Ghiara P, et al.1996), resulting in gastrointestinal disorders after helicobacter pylori infection.
The current treatment for helicobacter pylori infection usually involves the administration of the following drugs in combination: (1) antibiotics, such as: amoxicillin, clarithromycin, metronidazole, etc.; (2) bismuth salt (bismuth); (3) acid suppressors, proton pump inhibitors (proton pump inhibitors), and the like. However, since helicobacter pylori is likely to have resistance to antibiotics, at present, two antibiotics are administered in combination with a three-in-one or four-in-one therapy such as bismuth salt or proton pump inhibitor; the main side effects of the medicines are abnormal taste, nausea, diarrhea, flatulence, headache, dizziness and other obvious side effects, and if a patient stops taking the medicines by self, the helicobacter pylori is easy to generate drug resistance. In general, about 10-20% of patients have failed to eradicate H.pylori infection for the above reasons, and thus there is still room for improvement in the treatment of H.pylori infection.
Lactic acid bacteria (probiotics) are microorganisms that have been found to be beneficial to human health through research, and among them, the most widely used are the genus Lactobacillus (spp.) and the genus Bifidobacterium (Bifidobacterium spp.). In the adjuvant treatment of helicobacter pylori infections, it has been found in recent years that the clearance of helicobacter pylori by antibiotic therapy can be increased by using specific lactic acid bacteria strains, especially when the effects of three-in-one therapy are poor (Dang Y, Reinhardt JD, Zhou X and Zhang g.2014). In addition, studies have shown that the use of lactic acid bacteria can also reduce side effects caused by antibiotic therapy, including nausea, gastrointestinal upset, vomiting, etc. (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, it is a problem to be solved in the art to find a novel lactic acid bacteria composition to replace antibiotics for the treatment of helicobacter pylori infection.
Disclosure of Invention
In view of the above, the present inventors have deeply understood the shortcomings and drawbacks of the prior art, and have earnestly studied to improve the innovation and successfully develop a lactic acid bacteria composition for inhibiting helicobacter pylori.
In order to achieve the above object, the present invention provides a pharmaceutical composition for inhibiting gastritis induced by helicobacter pylori, comprising Lactobacillus selected from the group consisting of Lactobacillus rhamnosus GM-020 (also referred to as GMNL-74), Lactobacillus acidophilus GMNL-185 (Lactobacillus acidophilus), Lactobacillus plantarum GMNL-662 (Lactobacillus plantarum) GMNL-662 (Lactobacillus rhamnophilus), and Lactobacillus plantarum GMNL-662 (Lactobacillus plantarum) M2016571.
Wherein the pharmaceutical composition is in a dosage form for oral administration, and the dosage form is selected from the group consisting of a solution, a suspension, an emulsion, a powder, a lozenge, a pill, a syrup, a lozenge, a tablet, a chewing gum, a syrup, and a capsule.
To achieve the above object, the present invention provides another food product comprising probiotic Lactobacillus rhamnosus GM-020, Lactobacillus acidophilus GMNL-185 and Lactobacillus plantarum GMNL-662 and an edible material.
Wherein the edible material is selected from the group consisting of water, fluid dairy, concentrated milk, yogurt, frozen yogurt, lactobacillus fermented beverages, milk powder, ice cream, cheese, soy milk, fermented soy milk, fruit juice, sports drinks, desserts, jellies, candies, baby food, health food, animal feed, herbal compositions, and dietary supplements.
To achieve the above objects, the present invention provides another method for preparing a composition for treating helicobacter pylori infection, wherein the lactic acid bacteria is selected from the group consisting of Lactobacillus rhamnosus GM-020, Lactobacillus acidophilus GMNL-185, and Lactobacillus plantarum GMNL-662.
Wherein the lactobacillus can inhibit multiple drug resistance gastric helicobacter pylori and antibiotic sensitive helicobacter pylori by inhibiting gastric helicobacter pylori from adsorbing or invading gastric cells, inhibiting gastric helicobacter pylori induced interleukin-8 (IL-8) and NF-kB transcription factor, and inhibiting gastric COX-2 protein expression.
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FIG. 1 is a graph showing the arrangement of the adsorption force of 226 strains of lactic acid bacteria to human gastric epithelial cells (AGS);
FIG. 2A is a graph of IL-8 expression by ELISA;
FIG. 2B is a graph of NF-. kappa.B activity assayed by NF-. kappa.B-luminescence enzyme activity;
FIG. 3A is a graph of the analysis of the inhibition of helicobacter pylori adsorption of lactic acid bacteria on stomach cells;
FIG. 3B is a graph showing the inhibition of helicobacter pylori invasion of stomach cells by lactic acid bacteria;
FIG. 4A is a flowchart of mice fed H.pylori;
FIG. 4B is a graph showing the degree of infection of helicobacter pylori in gastric tissues analyzed by CLO test;
FIG. 4C is a graph showing the expression of COX-2, a gastric tissue inflammatory protein, analyzed by immunohistochemical analysis.
Detailed Description
All technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which this invention belongs, unless otherwise defined.
The terms "carrier", "excipient" and "diluent" as used herein refer to a non-toxic compound or agent that functions to assist the absorption of a drug into cells or tissues.
The composition used in the invention can be further added with an edible material to prepare a food product or a health-care product. Wherein the edible material comprises, but is not limited to: water (water), fluid milk products (fluid milk products), milk (milk), concentrated milk (concentrated milk); fermented milks (fermented milks), such as yogurt (yogurt), yogurt (sour milk), frozen yogurt (yogurt), fermented milk-based beverages (lactic acid bacteria-fermented beverages); milk powder (milk powder); ice cream (icecream); cheese (cheese); cheese (dry cheese); soymilk (soy milk); fermented soybean milk (fermented soybean milk); vegetable and fruit juices (vegetable-fruit juices); fruit juices (juices); sports drinks (sports drinks); dessert (confection); jelly (jellies); candies (confections); infant food (infant formula); health foods (health foods); animal feeds (animal feeds); chinese herbal medicines (Chinese herbases); dietary supplements (dietary supplements), and the like.
The aforementioned composition used in the present invention may be a dietary supplement and may be administered to the user in the following manner: mixing with a suitable drinkable liquid, such as water, yogurt, milk or fruit juice; or may be mixed with solid or liquid food products. In the present specification, the dietary supplement may be in the form of tablets, pills, capsules, dragees (lozenes), granules, powders, suspensions, sachets, pastilles, candies, syrups and corresponding administration forms, typically in unit dose form, and manufactured in a conventional manner for preparing dietary supplements.
The lactic acid bacteria used in the present invention are culture solutions of dead bacteria or live bacteria.
The following examples are illustrative only, and dosages may vary depending on variations, without limitation, the activity of the compound employed, the disease or physiological state being treated, the mode of administration, the individual requirements, the severity of the disease, and the judgment of the practitioner.
Example one screening for lactic acid bacteria highly adsorptive to human gastric cells (AGS)
Human gastric epithelial cell AGS (ATCC CRL1739) and activated lactobacillus bacterial solution (the bacterial infection dose MOI is 100) were cultured together for 2 hours, and then unadsorbed cells were washed with PBS and stained with Giemsa stain. The number of lactic acid bacteria adsorbed on human gastric epithelial cells (AGS) was observed under a microscope to evaluate the strength of adsorption of the strains.
FIG. 1 shows that more than 40 of the lactic acid bacterial strains adsorbed to the cells (shown as A in FIG. 1) under the oil-scope observation, and represented by "+ + + + +", showed the strongest binding to the cells; more than 20 lactic acid bacterial strains were adsorbed on the cells (as shown in B in FIG. 1), indicated by "+ +"; more than 10 lactic acid bacterial strains were adsorbed on the cells (as shown in C in FIG. 1), indicated by "+"; more than 3 lactic acid bacterial strains were adsorbed on the cells (as shown in D in FIG. 1), and are represented by "+"; if no lactic acid bacterial strain is adsorbed on the cell (as shown in E in FIG. 1), it is represented by "-", which means that there is no ability to bind to the cell.
Finally, the ability of 226 lactic acid bacteria to bind to human gastric epithelial cells (AGS) was analyzed, 18 lactic acid bacteria with the highest binding ability were selected (F in FIG. 1, marked with "+ + +") and compared with their gastric acid resistance, and 13 strains of lactic acid bacteria with higher gastric acid resistance were selected and further screened against helicobacter pylori.
Example II screening of lactic acid bacteria highly inhibiting IL-8 secretion induced by helicobacter pylori and inflammatory response associated with NF-. kappa.B transcription factor
The gastric epithelial cells are infected with helicobacter pylori and cultured under lactic acid bacteria (13 strains selected in the previous step) containing different strains for 16 hours, then the expression of IL-8 is analyzed by an ELISA method, and after an NF-kB-luminescent enzyme (NF-kB luciferase) construct is transferred into the gastric epithelial cells, the lactic acid bacteria and the helicobacter pylori are added for culturing for 12 hours together, the activity of the NF-kB-luminescent enzyme is analyzed, so that the activity of inflammatory reaction caused by the helicobacter pylori can be known, and whether the lactic acid bacteria have inhibition effect or not is further analyzed.
As shown in the first Table, it is clear that three strains, i.e., Lactobacillus rhamnosus GM-020 (also referred to as GMNL-74, shown as GMNL-74 in the table), Lactobacillus acidophilus GMNL-185, and Lactobacillus plantarum GMNL-662, have better IL-8 secretion inhibiting ability and NF- κ B production inhibiting effect than lactic acid bacteria of different strains of the same species.
TABLE I lactic acid bacteria screening results for inhibition of helicobacter pylori-induced inflammation-associated factors
Figure BDA0001704734780000061
The three lactic acid bacteria selected from the above table have the registration numbers, the registration dates, and the strain names shown in the second table.
TABLE II registration number of Lactobacillus in China
Figure BDA0001704734780000062
The gastric epithelial cells were infected with helicobacter pylori and cultured for 16 hours in the presence of lactic acid bacteria containing different strains (13 strains selected in the previous step), and then the expression level of IL-8 was analyzed by ELISA, and the results are shown in FIG. 2, which shows that the three strains selected from Table one are the three strains that are the most effective for inhibiting helicobacter pylori, and the three strains have statistical significance compared to the test group (HP) (. about.P < 0.01). FIG. 2A shows the expression of IL-8 and statistical analysis of the expression of IL-8, which indicates that three strains can inhibit the immune chemokine IL-8; FIG. 2B shows the relative activity of NF-. kappa.B transcription factors, and statistical analysis shows that three strains can inhibit the production of NF-. kappa.B transcription factor in the inflammatory pathway. From the above results, the inhibitory intensity of the three strains is slightly different, which means that the three strains can reduce the infiltration of immunocytes into the stomach and reduce the severity of local inflammatory reaction promotion by inhibiting the production of the immunochemical hormone IL-8 and the inflammatory reaction pathway transcription factor NF-kappa B.
Example three, three selected lactic acid bacteria strains have the activity of inhibiting helicobacter pylori adhesion (adhesion) and invasion (invasion) of gastric epithelial cells
To further confirm whether or not lactic acid bacteria have the ability to inhibit adsorption (adsorption) of helicobacter pylori to gastric epithelial cells. In the presence of lactic acid bacteria, H.pylori infected human gastric epithelial cells (AGS cells, ATCC CRL1739) at a bacterial infection dose of 100 (MOI) for 6 hours. After washing the cells, the cells were disrupted with water and serially diluted before being inoculated into blood culture medium. After 3-4 days of culture, colony Counts (CFU) were counted, wherein a smaller CFU value indicates that the number of adhered cells of H.pylori was inhibited by lactic acid bacteria.
The ability of the lactic acid bacteria to influence the invasion of helicobacter pylori (invasion activity) into gastric epithelial cells is analyzed by a gentamicin protection test (gentamicin protection assay) method, and if CFU is reduced, the lactic acid bacteria have the effect of influencing the invasion of the helicobacter pylori into gastric epithelial cells. After infection, the cells are washed three times by PBS and acted on by gentamicin (gentamicin) with the concentration of 100 mu g/ml which is impermeable to the cells for 1.5 hours to kill helicobacter pylori (H.pylori) on the surface, after washing, the cells are broken by water, after serial dilution, the cells are inoculated in a blood culture medium, and after 3-4 days of culture, the number of helicobacter pylori colonies is counted.
FIG. 3A is an analysis of the ability of helicobacter pylori to adsorb gastric cells; FIG. 3B is a graph showing the analysis of the ability of helicobacter pylori to invade gastric cells, in which the ability of single-pure helicobacter pylori to adsorb and invade gastric cells was regarded as 100%, and statistical analysis was performed, and the results of the comparative analysis were statistically significant in comparison with the experimental group (HP) (. about.P < 0.01).
The results show that the three lactic acid bacteria can effectively reduce the absorption of the helicobacter pylori to the gastric epithelial cells, the inhibition degree can reach more than 90 percent (as shown in figure 3A), and the invasion of the helicobacter pylori to the epithelial cells can be more effectively reduced, and the inhibition degree can be improved to more than 99 percent (as shown in figure 3B). The three strains show that the three strains have good effects on inhibiting the helicobacter pylori from adsorbing and invading epithelial cells. In addition, the inhibitory intensity of the three strains is slightly different under the two analysis platforms, so the use of the composite strain should be a better strategy.
Example four and three lactic acid bacteria combinations having the effect of additively inhibiting antibiotic-sensitive HP or multidrug-resistant HP strains
The ability of lactic acid bacteria to resist helicobacter pylori strains was analyzed by agar-well diffusion method (agar-well diffusion method) and bacteriostatic test. The h.pyri pathogenic strains used comprise: pylori BCRC 26695(ATCC 700392): wild-type strain (wild-type strain), sensitive to both the antibiotics metronidazole (metronidazole) and clarithromycin (clarithromycin); h.pyrori v 633: resistance to the antibiotic Metronidazole (MZ)R) And Clarithromycin (CH)R) (ii) a H.pyrori v2311: resistance to the antibiotic Metronidazole (MZ)R) But is sensitive to Clarithromycin (CH)S). Pyhori was placed under microaerobic conditions (85% N)2,10%CO2,5%O2) And culturing in Brucella Blood Agar Plate (BAP) culture medium, scraping off pathogenic bacteria, and adjusting concentration of pathogenic bacteria to 1 × 10 with Phosphate Buffer Solution (PBS)9cells/ml, 100. mu.l of diluted H.pyri was spread evenly on a quantitative BAP culture dish, left to stand for 15 minutes until the surface of the medium was dried, and a hole was dug in the above BAP medium coated with the bacterial solution using a glass tube with a diameter of 11 mm.
The bacteriostatic ability of lactic acid bacteria was confirmed by comparing the bacteriostatic effect of the whole cell suspension and the supernatant from which the cells were removed, and whether the bacteriostatic ability of lactic acid bacteria was derived from the surface material of the cells or the secretory material of the cells. The method for collecting the whole bacterial liquid comprises the following steps: activating GM-020, GMNL-185 and GMNL-662 overnight, culturing to MRS broth with 1% inoculum size, culturing for 18 hours, collecting whole bacteria liquid, and preparing mixed whole bacteria liquid (the ratio of three bacteria is 1:1: 1); the collection method for eliminating the thallus supernatant comprises the following steps: activating GM-020, GMNL-185 and GMNL-662 overnight, culturing the activated GM-020, GMNL-185 and GMNL-662 in MRS broth culture medium with 1% inoculum size twice, culturing for 18 hours, collecting the whole bacterial liquid, centrifuging the bacterial liquid at 13000rpm for 3 minutes, removing the bacterial cells, filtering the supernatant by a 0.45 mu m filter membrane to obtain a supernatant, and preparing the mixed supernatant at the same time (the ratio of the three bacterial strains is 1:1: 1).
And finally, in the bacteriostasis test, adding 100 mu l of lactobacillus test sample into the hole, carefully translating the culture disc to culture under microaerobic conditions at 37 ℃, observing the size of a bacteriostasis zone after 48 hours, and measuring the size in the bacteriostasis zone by using an electronic optical scale. And statistically analyzed by Student's t-test. P <0.05 indicated significant differences to confirm whether the mixed strains performed better than the single strains.
As can be seen from the results, either the gastric H.pylori strains (HP weld type, antibiotic sensitive) or the gastric H.pylori strains with single or multiple drug resistance (HP v2311: MZ)R;HP v633:MZR、CHR) GM-020 (also called GMNL-74, presented as GMNL-74 in the table), GMNL-185, GMNL-662 whole bacterial liquid or supernatant after eliminating bacterial cells all have obvious bacteriostatic ability, but the ability of inhibiting each pathogenic bacterium is different (as shown in the third and fourth tables); the bacteriostatic ability of the whole bacterial liquid is better than that of the supernatant, which shows that both the surface substances and the secretion substances of the thalli have the ability of inhibiting the helicobacter pylori; more particularly, the bacteriostatic ability of the lactic acid bacteria compositions of GM-020, GMNL-185 and GMNL-662 is obviously enhanced compared with that of a single bacterial strain (P)<0.05), which shows that the lactobacillus composition can enhance the effect of resisting helicobacter pylori, and simultaneously the composition can simultaneously have good inhibition effect on various clinical drug-resistant strains, and is not limited by clinical treatment with antibiotics.
TABLE III, results of inhibiting the zone of inhibition of helicobacter pylori by the whole bacterial liquid of lactic acid bacteria strains
Figure BDA0001704734780000091
Note that the mixed bacteria is a mixture of GM-020(GMNL-74), GMNL-185 and GMNL-662.
TABLE IV results of inhibition of the zone of inhibition of H.pylori by the supernatant of the lactic acid bacteria strains
Figure BDA0001704734780000092
Note that the mixed bacteria is a mixture of GM-020(GMNL-74), GMNL-185 and GMNL-662.
In the fifth embodiment, the combination of three lactic acid bacteria can obviously reduce the degree of H.pyrori infecting the stomach tissue of mice and reduce the stomach inflammation reaction
The protective effect of the lactic acid bacteria composition was evaluated by analyzing the inflammatory response of mice using a helicobacter pylori mouse test model experiment. Six week old BALB/c mice were divided into three groups: the first group was a control group (Mock), the second group was an experimental group (inoculated with H.pylori), and the third group was a daily tube-fed lactic acid bacteria composition (GM-020+ GMNL-185+ GMNL-662). Each group of experimental mice was fed with water or lactic acid bacteria (third group) in advance every day, and the amount of lactic acid bacteria was 2.4X 107CFU/time/mouse, continued until day 24. The experimental mice (second and third groups) were inoculated with H.pylori (shown in FIG. 4A) in the afternoon of 8 th, 10 th, 12 th, 14 th, 16 th, and 18 th days, six times in total, each at a bacterial count of 1X 109CFU/time/mouse. Stopping inoculating helicobacter pylori when the feed is fed to the eighteenth day, and continuing to feed the lactic acid bacteria.
Sacrificing the mice on day 25, taking stomach tissues and analyzing the activity of helicobacter pylori urease by using CLO (Campybacter-like Organism Test), wherein if the CLO Test culture medium is red to pink, the positive reaction is represented that the mice are still infected with helicobacter pylori in the stomach; if yellow color appears, a negative reaction is indicated, the quantified color is plotted in a histogram (as shown in FIG. 4B), and statistical analysis is performed, whereby whether the lactic acid bacteria composition can inhibit the infection of helicobacter pylori is analyzed. The CLO test results are shown in FIG. 4B, and it was found that the gastric CLO scores of the group of mixed tube-fed strains (GM-020+ GMNL-185+ GMNL-662) were significantly lower than those of the group inoculated with helicobacter pylori alone, and statistically significant compared to the experimental group (HP) (. about.P < 0.05).
The possible mechanism was presumed by analyzing the expression of the inflammatory factor cyclooxygene-2 (COX-2) in stomach tissue using immunohistochemical staining and background H & E staining to evaluate the inflammatory response of the stomach in the presence of lactic acid bacteria against helicobacter pylori infection.
The results in FIG. 4C show that feeding the mixed strains significantly inhibited COX-2 protein expression.
In conclusion, the invention screens out a Lactobacillus composition for resisting helicobacter pylori by screening 226 strains of Lactobacillus, wherein the Lactobacillus composition comprises Lactobacillus rhamnosus GM-020, Lactobacillus acidophilus GMNL-185 and Lactobacillus plantarum GMNL-662, and the Lactobacillus composition not only has the capability of highly combining to stomach cells, but also has the functions of reducing immune chemotaxis and promoting inflammatory reaction caused by the infection of the helicobacter pylori; in addition, the lactobacillus composition can effectively inhibit the absorption and invasion of gastric helicobacter pylori to stomach cells, has the effect of inhibiting a plurality of helicobacter pylori strains in an addition mode compared with a single strain, and is very helpful for treating the clinically-appearing antibiotic-resistant helicobacter pylori strains.
In addition, the whole bacterial liquid and the supernatant both have the effect of inhibiting the helicobacter pylori strains, and the effect of inhibiting the helicobacter pylori of the whole bacterial liquid is better than that of the supernatant, which shows that GM-020, GMNL-185 and GMNL-662 bacterial surface substances and bacterial secretion substances have the capacity of inhibiting the gastric helicobacter pylori. Furthermore, the lactic acid bacteria composition can reduce the secretion of the immune chemotactic cytokine IL-8 caused by helicobacter pylori and reduce the increase of the proinflammatory transcription factor NF-kB, and can also reduce the increase of the inflammation reaction of stomach COX-2 caused by the helicobacter pylori, and the result shows that the lactic acid bacteria composition can be used for preventing or treating the subsequent diseases caused by a large amount of stomach helicobacter pylori infection, such as: gastric ulcer, duodenal ulcer, chronic gastritis, gastric cancer and the like, and the characteristics of safety and no side effect of the lactobacillus composition, so the lactobacillus composition can be used as another excellent choice for treating diseases related to gastric helicobacter pylori infection.
The above-described embodiments are merely illustrative of the technical spirit and features of the present invention, and the object of the present invention is to enable those skilled in the art to understand the content of the present invention and to implement the same, and the scope of the present invention should not be limited by the claims, i.e. all equivalent changes and modifications made in the spirit of the present invention should be covered by the scope of the present invention.
[ depositing of biological Material ]
According to the registered country, organization, date and number sequence notes
GM-020, China center for type culture Collection, deposited date of 2003, 12 months and 18 days, deposited number of M203098, CCTCC NO.
GMNL-662 China, China center for type culture Collection, 2016, 10, 17 and CCTCC NO: M2016571.
GMNL-185 China, China center for type culture Collection, registration date of 2017, 11 months and 3 days, registration number of CCTCC NO. M2017764.

Claims (12)

1. A Chinese medicinal composition for inhibiting helicobacter pyloriHelicobacter pylori, H. pylori) Lactobacillus acidophilus causing gastritis (Lactobacillus acidophilus) GMNL-185 with a preservation number of CCTCC NO: M2017764.
2. A pharmaceutical composition for inhibiting gastritis induced by gastric helicobacter pylori, characterized in that the active ingredient thereof is Lactobacillus acidophilus (A), (B), B, CLactobacillus acidophilus) GMNL-185, and the preservation number of the lactobacillus acidophilus GMNL-185 is CCTCC NO: M2017764.
3. The pharmaceutical composition of claim 2, wherein the active ingredient is Lactobacillus rhamnosus (L) Lactobacillus rhamnosusLactobacillus rhamnosus) GM-020 and Lactobacillus acidophilus (Lactobacillus acidophilus) GMNL-185 and Lactobacillus plantarum: (Lactobacillus plantarum) A group of GMNL-662 combinations; the preservation number of the lactobacillus rhamnosus GM-020 is CCTCC NO: M203098, the preservation number of the lactobacillus acidophilus GMNL-185 is CCTCC NO: M2017764, and the preservation number of the lactobacillus plantarum GMNL-662 is CCTCC NO: M2016571.
4. The pharmaceutical composition of claim 2 or 3, wherein the pharmaceutical composition is in a form for oral administration.
5. The pharmaceutical composition of claim 4, wherein the dosage form is selected from the group consisting of a solution, a suspension, an emulsion, a powder, a lozenge, a pill, a syrup, a lozenge, a tablet, a chewing gum, and a capsule.
6. The pharmaceutical composition of claim 2 or 3, wherein the pharmaceutical composition further comprises a pharmaceutically acceptable excipient, diluent.
7. Use of lactic acid bacteria for the preparation of a composition for the treatment of helicobacter pylori infection in the stomach, wherein the lactic acid bacteria lactobacillus acidophilus is (Lactobacillus acidophilus) GMNL-185, and the preservation number of the lactobacillus acidophilus GMNL-185 is CCTCC NO: M2017764.
8. The use of claim 7, wherein the lactic acid bacteria in the composition are Lactobacillus rhamnosus (L.) (II.)Lactobacillus rhamnosus) GM-020 and Lactobacillus acidophilus (Lactobacillus acidophilus) GMNL-185 and Lactobacillus plantarum (Lactobacillus plantarum) A group of GMNL-662 combinations; the preservation number of the lactobacillus rhamnosus GM-020 is CCTCC NO: M203098, the preservation number of the lactobacillus acidophilus GMNL-185 is CCTCC NO: M2017764, and the preservation number of the lactobacillus plantarum GMNL-662 is CCTCC NO: M2016571.
9. The use according to claim 7 or 8, wherein the lactic acid bacteria are administered to inhibit the absorption or invasion of helicobacter pylori into the stomach cells to achieve the effect of inhibiting helicobacter pylori.
10. The use according to claim 7 or 8, wherein said lactic acid bacteria are further capable of inhibiting helicobacter pylori-induced mediator protein-8 (IL-8) and NF- κ B transcription factor.
11. Use according to claim 7 or 8, wherein said lactic acid bacteria are further capable of inhibiting gastric COX-2 protein expression.
12. Use according to claim 7 or 8, wherein the gastric helicobacter pylori is a multidrug-resistant helicobacter pylori strain or an antibiotic-sensitive helicobacter pylori strain.
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