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Abstract
Background: Nonalcoholic steatohepatitis (NASH) is characterized by liver steatosis, inflammation, and even fibrosis. NASH is likely to develop into cirrhosis and liver cancer, the major causes of liver related deaths. We aimed to study the effect of probiotics on NASH via the gut-liver axis.
Methods: Thirty male Sprague–Dawley rats were divided into three groups. A control group of 10 rats was fed on a standard chow for 16 weeks. Twenty rats fed on a high-fat diet for 8 weeks were separated to two groups: a model group (10 rats) fed on vehicle for 8 weeks and a treatment group (10 rats) supplemented with binary Bacillus subtilis for 8 weeks. Hepatic expression of IL-6 and TNF-ɑ and ileum expression of IL-17 and occludin were measured.
Results: The high-fat diet caused inflammation of the liver and ileum in rats. Binary Bacillus subtilis treatment reduces liver inflammation through the intestinal liver axis. Increased levels of IL-6 and TNF-α were detected in rats fed a high-fat diet, which were reduced to lower levels after treatment with binary Bacillus subtilis. In rats on the high-fat diet, elevated IL-17 levels and decreased occludin levels were observed. Treatment with Bacillus subtilis reduced IL-17 levels and restored the expression of occludin.
Conclusion: Binary Bacillus subtilis has a beneficial effect on liver inflammation and intestinal damage.
Keywords
non-alcoholic steatohepatitis
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Donglin Liu, Pengguo Chen.
Binary Bacillus subtilis protects the intestinal mucosa barrier and alleviates nonalcoholic steatohepatitis.
Animal Models and Experimental Medicine, 2024, 7(3): 362-366 DOI:10.1002/ame2.12337
| [1] |
Younossi ZM, Loomba R, Rinella ME, et al. Current and future therapeutic regimens for nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Hepatology. 2018;68(1):361-371.
|
| [2] |
Ajmera V, Loomba R. Imaging biomarkers of NAFLD, NASH, and fibrosis. Mol Metab. 2021;50:101167.
|
| [3] |
Kasper P, Martin A, Lang S, et al. NAFLD and cardiovascular diseases: a clinical review. Clin Res Cardiol. 2021;110:921-937.
|
| [4] |
Albillos A, de Gottardi A, Rescigno M. The gut-liver axis in liver disease: pathophysiological basis for therapy. J Hepatol. 2020;72(3):558-577.
|
| [5] |
Tremaroli V, Backhed F. Functional interactions between the gut microbiota and host metabolism. Nature. 2012;489(7415):242-249.
|
| [6] |
Brown K, Godovannyi A, Ma C, et al. Prolonged antibiotic treatment induces a diabetogenic intestinal microbiome that accelerates diabetes in NOD mice. ISME J. 2016;10(2):321-332.
|
| [7] |
Compare D, Coccoli P, Rocco A, et al. Gut-liver axis: the impact of gut microbiota on non alcoholic fatty liver disease. Nutr Metab Cardiovasc Dis. 2012;22(6):471-476.
|
| [8] |
Sharpton SR, Maraj B, Harding-Theobald E, Vittinghoff E, Terrault NA. Gut microbiome-targeted therapies in nonalcoholic fatty liver disease: a systematic review, meta-analysis, and meta-regression. Am J Clin Nutr. 2019;110:139-149.
|
| [9] |
Meroni M, Longo M, Dongiovanni P. The role of probiotics in nonalcoholic fatty liver disease: a new insight into therapeutic strategies. Nutrients. 2019;11:2642.
|
| [10] |
Li Z, Yang S, Lin H, et al. Probiotics and antibodies to TNF inhibit inflammatory activity and improve nonalcoholic fatty liver disease. Hepatology. 2003;37:343-350.
|
| [11] |
Chen P, Li J, Huo Y, et al. Adenovirus-mediated expression of orphan nuclear receptor NR4A2 targeting hepatic stellate cell attenuates liver fibrosis in rats. Sci Rep. 2016;6:33593.
|
| [12] |
Chen P, Li J, Huo Y, et al. Orphan nuclear receptor NR4A2 inhibits hepatic stellate cell proliferation through MAPK pathway in liver fibrosis. PeerJ. 2015;3:e1518.
|
| [13] |
Li J, Sung CY, Lee N, et al. Probiotics modulated gut microbiota suppresses hepatocellular carcinoma growth in mice. Proc Natl Acad Sci USA. 2016;113(9):E1306-E1315.
|
| [14] |
Dörfel MJ, Huber O. Modulation of tight junction structure and function by kinases and phosphatases targeting occludin. J Biomed Biotechnol. 2012;2012:807356.
|
| [15] |
Bessone F, Razori MV, Roma MG. Molecular pathways of nonalcoholic fatty liver disease development and progression. Cell Mol Life Sci. 2019;76:99-128.
|
| [16] |
Rahman K, Desai C, Iyer SS, et al. Loss of junctional adhesion molecule a promotes severe steatohepatitis in mice on a diet high in saturated fat, fructose, and cholesterol. Gastroenterology. 2016;151(4):733-746.e12.
|
| [17] |
Leung C, Rivera L, Furness JB, Angus PW. The role of the gut microbiota in NAFLD. Nat Rev Gastroenterol Hepatol. 2016;13(7):412-425.
|
| [18] |
Jiang W, Wu N, Wang X, et al. Dysbiosis gut microbiota associated with inflammation and impaired mucosal immune function in intestine of humans with non-alcoholic fatty liver disease. Sci Rep. 2015;5:8096.
|
| [19] |
Betrapally NS, Gillevet PM, Bajaj JS. Changes in the intestinal microbiome and alcoholic and nonalcoholic liver diseases: causes or effects? Gastroenterology. 2016;150:1745-1755.e3.
|
| [20] |
Aron-Wisnewsky J, Dore J, Clement K. The importance of the gut microbiota after bariatric surgery. Nat Rev Gastroenterol Hepatol. 2012;9:590-598.
|
| [21] |
Peterson LW, Artis D. Intestinal epithelial cells: regulators of barrier function and immune homeostasis. Nat Rev Immunol. 2014;14:141-153.
|
| [22] |
Luther J, Garber JJ, Khalili H, et al. Hepatic injury in nonalcoholic steatohepatitis contributes to altered intestinal permeability. Cell Mol Gastroenterol Hepatol. 2015;1(2):222-232.
|
| [23] |
Matsumoto K, Ichimura M, Tsuneyama K, et al. Fructo-oligosaccharides and intestinal barrier function in a methionine-choline-deficient mouse model of nonalcoholic steatohepatitis. PLoS One. 2017;12(6):e0175406.
|
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2023 The Author(s). Animal Models and Experimental Medicine published by John Wiley & Sons Australia, Ltd on behalf of The Chinese Association for Laboratory Animal Sciences