CN114652753B - Application of bifidobacterium bifidum B11 in preparation of products for inhibiting helicobacter pylori and repairing gastric mucosa barrier - Google Patents
Application of bifidobacterium bifidum B11 in preparation of products for inhibiting helicobacter pylori and repairing gastric mucosa barrier Download PDFInfo
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- CN114652753B CN114652753B CN202210476136.4A CN202210476136A CN114652753B CN 114652753 B CN114652753 B CN 114652753B CN 202210476136 A CN202210476136 A CN 202210476136A CN 114652753 B CN114652753 B CN 114652753B
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- A—HUMAN NECESSITIES
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- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K35/00—Medicinal preparations containing materials or reaction products thereof with undetermined constitution
- A61K35/66—Microorganisms or materials therefrom
- A61K35/74—Bacteria
- A61K35/741—Probiotics
- A61K35/744—Lactic acid bacteria, e.g. enterococci, pediococci, lactococci, streptococci or leuconostocs
- A61K35/745—Bifidobacteria
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- A—HUMAN NECESSITIES
- A23—FOODS OR FOODSTUFFS; TREATMENT THEREOF, NOT COVERED BY OTHER CLASSES
- A23L—FOODS, FOODSTUFFS, OR NON-ALCOHOLIC BEVERAGES, NOT COVERED BY SUBCLASSES A21D OR A23B-A23J; THEIR PREPARATION OR TREATMENT, e.g. COOKING, MODIFICATION OF NUTRITIVE QUALITIES, PHYSICAL TREATMENT; PRESERVATION OF FOODS OR FOODSTUFFS, IN GENERAL
- A23L33/00—Modifying nutritive qualities of foods; Dietetic products; Preparation or treatment thereof
- A23L33/10—Modifying nutritive qualities of foods; Dietetic products; Preparation or treatment thereof using additives
- A23L33/135—Bacteria or derivatives thereof, e.g. probiotics
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- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P1/00—Drugs for disorders of the alimentary tract or the digestive system
- A61P1/04—Drugs for disorders of the alimentary tract or the digestive system for ulcers, gastritis or reflux esophagitis, e.g. antacids, inhibitors of acid secretion, mucosal protectants
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- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P31/00—Antiinfectives, i.e. antibiotics, antiseptics, chemotherapeutics
- A61P31/04—Antibacterial agents
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- C12N1/00—Microorganisms, e.g. protozoa; Compositions thereof; Processes of propagating, maintaining or preserving microorganisms or compositions thereof; Processes of preparing or isolating a composition containing a microorganism; Culture media therefor
- C12N1/20—Bacteria; Culture media therefor
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- A23V—INDEXING SCHEME RELATING TO FOODS, FOODSTUFFS OR NON-ALCOHOLIC BEVERAGES AND LACTIC OR PROPIONIC ACID BACTERIA USED IN FOODSTUFFS OR FOOD PREPARATION
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- A—HUMAN NECESSITIES
- A23—FOODS OR FOODSTUFFS; TREATMENT THEREOF, NOT COVERED BY OTHER CLASSES
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Abstract
The invention relates to the technical field of microorganisms, in particular to application of bifidobacterium bifidum B11 with the preservation number of CGMCC No.24381 in preparing products for inhibiting helicobacter pylori and repairing gastric mucosa barrier. The bifidobacterium bifidum B11 provided by the invention has a remarkable inhibiting effect on helicobacter pylori and a strong adhesion effect with gastric cancer cell AGS, provides possibility for the bifidobacterium bifidum B11 to adhere to gastric epithelial cells and peripheral mucus layers thereof, enables the bifidobacterium bifidum B11 to have the potential of permanent planting in the stomach, can remarkably inhibit the adhesion of the helicobacter pylori on the gastric epithelial cells, and simultaneously, the bifidobacterium bifidum B11 can inhibit the transcription level of a proinflammatory factor IL-8, inhibit inflammation caused by the helicobacter pylori and play a role in protecting the gastric mucosa. Meanwhile, the live strain of the strain can promote the transcription of mucosa protection factors TFF1, iNOS and COX-2, and has positive effects on gastric mucosa barrier and cell repair.
Description
Technical Field
The invention relates to the technical field of microorganisms, in particular to application of bifidobacterium bifidum B11 in preparing products for inhibiting helicobacter pylori and repairing gastric mucosa barrier.
Background
Helicobacter pylori, also known as helicobacter pylori, called Hp for short, of the genus latin, is a gram-negative, microaerophilic bacterium that lives in the stomach and duodenum in various regions. It can cause slight chronic inflammation of gastric mucosa, or even gastric and duodenal ulcers and gastric cancer, and is determined as the type I carcinogenic factor by the world health organization, so that the research on preventing and treating helicobacter pylori has great application value.
With the increase of a plurality of factors such as strain variation, secondary drug resistance, cross infection of different strains and the like, the eradication rate of the helicobacter pylori is reduced year by year. Meanwhile, when the antibiotics are used for treating helicobacter pylori infection, irregular abuse of the antibiotics can generate adverse effects on a gastrointestinal microecological system, destroy the gastrointestinal microecological balance and a microbial barrier, gradually reduce antibacterial drug sensitive strains in intestinal tracts, increase the drug resistant strains, and cause a plurality of adverse reactions of part of patients, such as abdominal pain, nausea, vomiting, diarrhea and the like, and generate an increasing trend. Research shows that probiotics has the effect of inhibiting helicobacter pylori, but probiotics on the market at present have poor effect of inhibiting the helicobacter pylori, so that the development of probiotics capable of effectively inhibiting the helicobacter pylori, improving gastrointestinal discomfort and improving the clinical treatment effect of helicobacter pylori infection is necessary.
Disclosure of Invention
Aiming at the defects in the prior art, the invention provides the application of bifidobacterium bifidum B11 in inhibiting helicobacter pylori and repairing gastric mucosa barrier, the living strain or metabolite of the strain can inhibit the growth of helicobacter pylori, adhere gastric cancer cells, inhibit the adhesion of helicobacter pylori to gastric cancer cells and eliminate inflammation caused by helicobacter pylori, and meanwhile, the living strain of the strain can also repair the gastric mucosa barrier and promote the transcription of mucosa protection factors.
In order to achieve the purpose, the invention adopts the following technical scheme:
application of Bifidobacterium bifidum B11 with preservation number of CGMCC No.24381 in preparing products for inhibiting helicobacter pylori and repairing gastric mucosa barrier. The strain has been preserved in China general microbiological culture Collection center on 21.01.21.2022, the preservation address is No. 3 Xilu-Beijing institute of microbiology, Naja-Kogyo, Beijing.
The substances such as organic acid, bacteriocin and the like in the metabolite of the bifidobacterium bifidum B11 provided by the invention have obvious inhibition effect on helicobacter pylori, and the living bacterial strain has strong adhesion effect with gastric cancer cell AGS, has the potential of adhering to gastric epithelial cells and then colonizing the stomach, and provides possibility for the bifidobacterium bifidum B11 to play a role in inhibiting the helicobacter pylori through competitive inhibition. The test proves that the inhibiting rate of the bifidobacterium bifidum B11 for inhibiting the adhesion of helicobacter pylori on gastric epithelial cells can reach 17.8%. Meanwhile, the bifidobacterium bifidum B11 can also inhibit the transcription level of proinflammatory factor IL-8 and inhibit inflammation caused by helicobacter pylori, thereby protecting the gastric mucosa. The live strain of the strain can also promote the transcription of mucosa protective factors, namely trefoil peptide (TFF1), iNOS and COX-2, and has positive effects on gastric mucosa barrier and cell repair.
Preferably, when the product is a helicobacter pylori inhibiting product, the bifidobacterium bifidum B11 is a live strain or a metabolite thereof.
Preferably, the product is a product for inhibiting the growth of helicobacter pylori.
Preferably, the product is a product for adhering gastric cancer cells.
Preferably, the product is a product for inhibiting the adhesion of helicobacter pylori to gastric cancer cells.
Preferably, the product is a product for eliminating inflammation caused by helicobacter pylori.
Preferably, when the product is a product for repairing gastric mucosa barrier, the bifidobacterium bifidum B11 is a live strain.
Preferably, the product is a product for promoting transcription of a mucosal protective factor.
Preferably, the mucosal protective factor includes at least one of TFF1, iNOS, and COX-2.
The products for inhibiting helicobacter pylori and repairing gastric mucosa barrier comprise medicines, health-care foods or foods, the dosage forms of the medicines and the health-care foods comprise but are not limited to conventional dosage forms such as powder, tablets, capsules, granules or solutions, and the forms of the foods comprise but are not limited to beverages, cold cakes, dairy products and the like.
Drawings
FIG. 1 is a graph showing the inhibitory effect of Bifidobacterium bifidum B11 on helicobacter pylori as provided in example 1;
FIG. 2 is the adhesion of Bifidobacterium bifidum B11 to gastric cancer cell AGS as provided in example 2;
FIG. 3 is a graph showing that Bifidobacterium bifidum B11 provided in example 3 inhibits adhesion of helicobacter pylori to gastric cancer cells;
FIG. 4 is a diagram showing the inhibition of H.pylori Hp-mediated secretion of IL-8 by Bifidobacterium bifidum B11 provided in example 4;
FIG. 5 is a graph showing the effect of Bifidobacterium bifidum B11 on transcription of mucosal protective factor TFF1 as provided in example 5;
FIG. 6 is a graph showing the effect of Bifidobacterium bifidum B11 on promoting transcription of the mucosal protective factors nitric oxide synthase iNOS and cyclooxygenase COX-2 provided in example 6.
Detailed Description
In order to make the objects, technical solutions and advantages of the present invention more apparent, the present invention is further described in detail with reference to the following embodiments. It should be understood that the specific embodiments described herein are merely illustrative of the invention and are not intended to limit the invention.
The probiotics on the market at present have poor inhibition effect on helicobacter pylori, and the bifidobacterium bifidum B11 with the preservation number of CGMCC No.24381 provided by the invention has the effects of inhibiting the helicobacter pylori and repairing the gastric mucosa barrier. On the first hand, bifidobacterium bifidum B11 has a remarkable inhibiting effect on the growth of helicobacter pylori, has a strong adhesion effect with gastric cancer cell AGS, has the potential of being planted in the stomach, can inhibit the adhesion of the helicobacter pylori on gastric epithelial cells through competitive inhibition, and meanwhile bifidobacterium bifidum B11 can inhibit the transcription level of a proinflammatory factor IL-8, inhibit inflammation caused by the helicobacter pylori and protect the gastric mucosa. In a second aspect, the live strain of Bifidobacterium bifidum B11 is also capable of promoting the transcription of mucosal protective factors TFF1, iNOS and COX-2, with positive effects on gastric mucosal barrier and cell repair.
The formulation of the modified MRS medium used in the following examples was: 20g of glucose, 10g of peptone, 6.5g of beef powder, 5g of yeast extract powder, 5g of sodium acetate, 2g of diammonium hydrogen citrate, 2g of dipotassium hydrogen phosphate and MgSO 4 ·7H 2 O 0.58g，MnSO 4 ·H 2 0.25g of O, 0.5g of cysteine hydrochloride, 801 mL of Tween and 1000mL of distilled water.
Example 1
This example provides the inhibitory effect of Bifidobacterium bifidum B11 on helicobacter pylori.
Activating Bifidobacterium bifidum B11 for 3 generations, inoculating in improved MRS culture medium, anaerobically culturing at 37 deg.C for 18 hr, and adjusting the density of the bacterial liquid to 1.0 × 10 8 Centrifuging at 4 deg.C and 5000r/min for 5min at CFU/mL, collecting the culture supernatant, and filtering with 0.22 μm filter membrane for sterilization.
Performing bacteriostatic test by Oxford cup method, pouring solid culture medium into plate, solidifying, suspending activated third generation stable passage helicobacter pylori with sterile PBS, and the bacterial concentration is about (1 × 10) 8 ) Add 1ml to the plateShaking evenly, standing for 3 minutes and drying in the air. Placing Oxford cup on a plate, adding 100 μ L of the filtered Bifidobacterium bifidum B11 culture supernatant into the well, culturing at 37 deg.C for 18h in anaerobic environment, observing and measuring the diameter of the inhibition zone, and modifying MRS culture medium as negative control.
As shown in FIG. 1, the inhibitory diameters of the negative control and Bifidobacterium bifidum B11 were 10.5. + -. 1.2mm and 14.8. + -. 1.7mm, respectively. The metabolite of Bifidobacterium bifidum B11 contains organic acids and bacteriocin, and has significant inhibitory effect on helicobacter pylori. The organic acid lactic acid can change the permeability of gram-negative bacteria cell membranes, and further improve the bacteriostatic effect. Since the lactic acid content in the metabolite is positively correlated with the degree of inhibition of helicobacter pylori, the culture supernatant of bifidobacterium bifidum B11 is known to have significant inhibition effect on the growth of helicobacter pylori according to the size of the inhibitory diameter in the figure.
Example 2
This example provides the adhesion of bifidobacterium bifidum B11 to gastric cancer cell AGS.
Digesting the AGS of adherent gastric cancer cells stably cultured for three generations by pancreatin, terminating the reaction, centrifugally washing, suspending by using nonresistant F12 (fetal bovine serum 10%) culture solution, and adjusting the concentration of the cell sap to 5 multiplied by 10 4 one/mL), and incubated overnight by allowing to stand. After the cells are fully paved on the glass slide, washing the glass slide for 3 times by using a PBS buffer solution; activating Bifidobacterium bifidum B11 for 3 generations, inoculating in improved MRS culture medium, anaerobically culturing at 37 deg.C for 18 hr, and adjusting the density of the bacterial liquid to 1.0 × 10 8 The cells were collected by centrifugation at 5000r/min at 4 ℃ under CFU/mL, and the concentration of the cells was adjusted to 1X 10 by using a nonresistant F12 (fetal bovine serum 10%) medium 8 And (4) immersing the adjusted bacterial liquid into the glass slide full of gastric cancer cell AGS for culturing for 3 hours, washing with PBS for three times, fixing for 2 hours by using a methanol fixing solution, and performing microscopic examination after gram staining.
The results are shown in fig. 2, bifidobacterium bifidum B11 has strong adhesion with gastric cancer cell AGS, and the bifidobacterium bifidum B11 is proved to have the potential of colonization in the stomach. Helicobacter pylori mainly colonizes on the surface of gastric epithelial cells and peripheral mucus layers thereof, and bifidobacterium bifidum B11 colonizes in the stomach and can exert the inhibition effect on the helicobacter pylori through competitive inhibition.
Example 3
This example provides the use of Bifidobacterium bifidum B11 for inhibiting the adhesion of helicobacter pylori to gastric cancer cells.
Digesting adherent gastric cancer cell AGS of continuous three-generation stable culture with pancreatin, terminating reaction, centrifuging, washing, suspending with nonresistant F12 (fetal calf serum 10%) culture solution, and adjusting cell sap concentration to 5 × 10 4 one/mL), 100. mu.L per well was inoculated into a 96-well plate and allowed to stand overnight at 37 ℃. After the cells were spread over the bottom of the well plate, they were washed 3 times with PBS buffer and the following different groups were set for co-incubation with gastric cancer cell AGS.
Control group: the activated third generation of helicobacter pylori was treated with nonresistant F12 (fetal bovine serum 10%) medium to adjust the concentration of the culture to 1X 10 8 Adding 100 mu L of improved MRS culture medium after adding 100 mu L of the mixture to be used as a control group;
test groups: activating Bifidobacterium bifidum B11 for 3 generations, inoculating in improved MRS culture medium, anaerobically culturing at 37 deg.C for 18 hr, and adjusting bacterial liquid density to 1.0 × 10 8 The cells were collected by centrifugation at 5000r/min at 4 ℃ under CFU/mL, and the concentration of the cells was adjusted to 1X 10 by using F12 (fetal bovine serum 10%) as a medium 8 Mixing Bifidobacterium bifidum B11 with helicobacter pylori suspension at a volume ratio of 1:1, and adding 200 μ L to obtain test group;
the control group and the test group samples are placed in a cell culture box, cultured for 3h at 37 ℃, washed three times by PBS, added with 50 mu L of urease test solution, and oscillated to measure the light absorption value by a 550nm enzyme-linked immunosorbent assay. As shown in FIG. 3, Bifidobacterium bifidum B11 could colonize the stomach by adhesion with gastric cancer cell AGS, inhibiting the adhesion of helicobacter pylori on gastric epithelial cells with an inhibition rate of 17.8%, and it can be seen that Bifidobacterium bifidum B11 could inhibit the amount of helicobacter pylori by competing with helicobacter pylori for the adhesion sites on the cells.
Example 4
This example provides the use of Bifidobacterium bifidum B11 for inhibiting the secretion of H.pylori Hp-mediated IL-8.
Gastric cancer cell AGS obtained by continuous three-generation stable culture was inoculated into a 24-well plate (inoculation concentration: 5X 10) 4 one/mL, culture volume 200 μ L/well), cultured at 37 ℃ for 24h, washed to remove dead AGS cells with non-resistant F12 (fetal bovine serum 10%) medium, and set up the following different groups incubated with gastric cancer cell AGS.
Blank control group (AGS): add 200. mu.L/well of non-resistant F12 (fetal bovine serum 10%) medium;
AGS + Hp group: 180. mu.L of non-resistant F12 (fetal bovine serum 10%) medium and 20. mu.L of H.pylori suspension (final cell concentration 1X 10) 8 one/mL);
AGS + Hp + B11 group: 160. mu.L of non-resistant F12 (fetal bovine serum 10%) medium and 20. mu.L of helicobacter pylori suspension (final cell concentration 1X 10) 8 One per mL) and 20. mu.L of Bifidobacterium bifidum B11 bacterial suspension (final concentration of bacterial cells 1X 10) 8 one/mL);
AGS + B11 group: adding non-resistant F12 (fetal calf serum 10%) culture medium 180 μ L, and Bifidobacterium bifidum B11 (final cell concentration 1 × 10) 8 one/mL);
incubated in an incubator at 37 ℃ for 4 h. Collecting bacterial liquid, centrifuging the bacterial liquid at 8000g for 10min, collecting precipitate, extracting RNA reverse cDNA for detection according to 2 -△△Ct Values the IL-8 transcript level was calculated.
As shown in FIG. 4, the infection of human body with H.pylori stimulates the production of various cytokines by gastric mucosal epithelial cells, resulting in increased IL-8 production and thus a series of inflammatory responses. Bifidobacterium bifidum B11 can inhibit the transcription level of proinflammatory factor IL-8, inhibit inflammation caused by helicobacter pylori, and protect gastric mucosa.
Example 5
The embodiment provides application of bifidobacterium bifidum B11 in promoting transcription of mucosal protective factor trefoil peptide (TFF1)
1. Preparing a cell suspension:
enzymolysis: digesting monolayer cultured gastric cancer cell AGS with trypsin, collecting suspension cultured cells, and making into single cell suspension with cell density of 10 4 one/mL.
Sample adding: sucking 40 mu L of the cell suspension and 40 mu L of 0.4% trypan blue solution, blowing, sucking, uniformly mixing and staining for 2min, covering the cover glass sheet between the two grooves of the counting plate, blowing the cell suspension by using a suction tube, sucking 20 mu L of the cell suspension, adding the cell suspension on one side of the cover glass on the counting plate, wherein the adding amount does not overflow the cover glass.
Counting: under a microscope, the number of cells in a square grid at the four corners of the counting plate is observed by a 10X objective lens, only the left side and the upper side are counted when the cells press the central line, and the right side and the lower side are not counted.
And (3) calculating: the cell density was obtained by substituting the calculation results into the following formula.
Cell count/ml stock solution (sum of 4 large cells/4) × 10 4 X dilution factor
2. Cell proliferation assay
According to the appropriate number of plated cells, the purified cells were seeded into 96-well plates at a density of 5X 10 4 one/mL, about 100. mu.L of cell suspension per well, 5 replicate wells per set, were incubated in a 37 ℃ incubator.
After cell inoculation, adherent culture is carried out for about 16h, the growth state of cells in each hole is observed by microscopic examination, when the growth density is close to 90%, 10 mu L of the culture medium with the density of 1 multiplied by 10 is added into each hole of an experimental hole 8 one/mL of Bifidobacterium bifidum B11 suspension was added to each well of the control well in an equal amount of non-resistant F12 (10% fetal bovine serum) medium and incubated at 37 ℃ in an incubator for 4 hours. Another 96-well plate which is not inoculated with AGS cells is taken, and 10 mu L of the AGS cells are added into each well of the experimental well, wherein the density of each well is 1 multiplied by 10 8 each/mL of Bifidobacterium bifidum B11 suspension was cultured in an incubator at 37 ℃ for 4 hours by adding an equal amount of non-resistant F12 (10% fetal bovine serum) to each well of the blank well.
The original medium was removed from each group and replaced with new medium, then 10. mu.L of CCK-8 solution was added to each well at a final concentration of 10 wt%, and the plates were gently tapped to aid in mixing. Culturing in a cell culture box for 1h, and measuring the detection result by using double wavelengths, wherein the detection wavelength is 450nm and the reference wavelength is 600 nm. And finally, subtracting the reference wavelength value from the detection wavelength value, and calculating the survival rate of the AGS cells by referring to a calculation formula. Calculating the formula:
cell survival rate ═ [ (As-Ab1)/(Ac-Ab) ] × 100%;
wherein As represents the absorbance of a test well (AGS cell-containing medium, CCK-8, Bifidobacterium bifidum B11);
ac represents the absorbance in the control well (AGS cell-containing medium, CCK-8);
ab represents the absorbance of a blank well (blank medium, CCK-8) not inoculated with AGS cells;
ab1 represents the absorbance of experimental wells (blank medium, CCK-8, Bifidobacterium bifidum B11) not inoculated with AGS cells.
3. TFF1 test:
gastric cancer cell AGS obtained by continuous three-generation stable culture was inoculated into a 24-well plate (inoculation concentration: 5X 10) 4 one/mL, culture volume 200 μ L) for 24h, washed dead AGS cells with non-resistant F12 (fetal bovine serum 10%) medium, and set up for 3 replicates of the following different groups of co-incubations with cells.
Blank control group (AGS): 200 μ L of non-resistant F12 (fetal bovine serum 10%) medium was added;
test group (AGS + B11): adding 180 μ L of non-resistant F12 (fetal calf serum 10%) culture medium and 20 μ L of Bifidobacterium bifidum B11 (final cell concentration 1 × 10) 8 one/mL);
incubate for 4h in an incubator at 37 ℃ while standing. Collecting bacterial liquid, centrifuging the bacterial liquid at 8000g for 10min, collecting precipitate, extracting RNA reverse cDNA for detection according to 2 -△△Ct The calculated transcription level is evaluated.
The gastric mucosa protective factor is important for protecting or repairing the gastric mucosa after damage. The Trefoil Factor Family (TFF), including three members of TFF1, TFF2 and TFF3, is mainly secreted from mucus secreting cells of human gastrointestinal tissues, and the expression of the TFF is related to mucin MUC secreting cells. The secretion of TFFs can promote the movement of epithelial cells of gastric mucosa, rapidly repair and prevent inflammation. The results of the above experiments are shown in fig. 5, bifidobacterium bifidum B11 can maintain cell activity, promote transcription of TFF1 factor, and further have positive effect on repair of gastric mucosal cells.
Example 6
This example provides the use of Bifidobacterium bifidum B11 in promoting transcription of the mucosal protective factors nitric oxide synthase iNOS and cyclooxygenase COX-2
Gastric cancer cell AGS obtained by continuous 3-generation culture was inoculated into 24-well plates (inoculation concentration: 5X 10) 4 one/mL, culture volume 200 μ L) for 24h, and dead AGS cells were washed out with non-resistant F12 (fetal bovine serum 10%) medium, setting up the following different groups to be co-incubated with the cells.
Blank control group (AGS): 200 μ L of non-resistant F12 (fetal bovine serum 10%) medium was added;
test group (AGS + B11): adding 180. mu.L of non-resistant F12 (fetal bovine serum 10%) culture medium and 20. mu.L of Bifidobacterium bifidum B11 bacterial suspension (final bacterial concentration of 1 × 10) 8 one/mL);
incubated in incubator for 4 h. Collecting bacterial liquid, centrifuging the bacterial liquid at 8000g for 10min, collecting precipitate, extracting RNA reverse cDNA for detection according to 2 -△△Ct Values, transcription levels of iNOS and COX-2 were calculated.
NO is produced by L-arginine (L-arg) catalyzed by Nitric Oxide Synthase (NOS). NOS is classified into endothelial type (eNOS), neural type (nNOS), and inducible type (iNOS), eNOS is mainly present in vascular endothelial cells, and its synthesized NO is mainly used to regulate and maintain GMBF, and plays an important role in defending injury factors and promoting gastric mucosal repair.
COX-2 has effects of repairing gastric mucosa and accelerating ulcer healing by synthesizing endogenous PGE 2. The PGE2 has the most content and strong biological activity, and plays a main protection role. Studies have demonstrated that PGE2 provides gastric cytoprotective effect against damage caused by gastric acid, ethanol, indomethacin, or acid reverse diffusion after the gastric mucosal barrier of rats is disrupted.
The results of the above experiments are shown in fig. 6, bifidobacterium bifidum B11 can promote the transcription of mucosa protective factors iNOS and COX-2, indicating that bifidobacterium bifidum B11 can have a positive effect on gastric mucosa barrier and cell repair.
The above description is only for the purpose of illustrating the preferred embodiments of the present invention and is not to be construed as limiting the invention, and any modifications, equivalents or improvements made within the spirit and principle of the present invention should be included in the scope of the present invention.
Claims (9)
1. Application of Bifidobacterium bifidum B11 with preservation number of CGMCC No.24381 in preparing products for inhibiting helicobacter pylori and repairing gastric mucosa barrier.
2. The use of claim 1, wherein: when the product is a product for inhibiting helicobacter pylori, the bifidobacterium bifidum B11 is a live strain or a culture supernatant thereof.
3. Use according to claim 2, characterized in that: the product is used for inhibiting the growth of helicobacter pylori.
4. Use according to claim 2, characterized in that: the product is used for adhering gastric cancer cells.
5. Use according to claim 2, characterized in that: the product is used for inhibiting helicobacter pylori from adhering to gastric cancer cells.
6. Use according to claim 2, characterized in that: the product is used for eliminating inflammation caused by helicobacter pylori.
7. The use of claim 1, wherein: when the product is a product for repairing gastric mucosa barrier, the bifidobacterium bifidum B11 is a viable strain.
8. The use of claim 7, wherein: the product is used for promoting the transcription of the mucosa protective factor.
9. The use of claim 8, wherein: the mucosa protective factor comprises at least one of TFF1, iNOS and COX-2.
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