Short‑chain fatty acid butyrate: A novel shield against chronic gastric ulcer

Abstract

Butyrate is one of the most abundant short-chain fatty acids produced by intestinal bacteria. In the present study, the action of butyrate on chronic gastric mucosa lesions was investigated, as well as its underlying mechanism in mice. Male mice from the Institute of Cancer Research were randomly divided into three groups: Sham, model and butyrate groups. Butyrate was administered intragastrically for 7 days to butyrate group mice following the establishment of a gastric ulcer model. Hematoxylin and eosin staining, immunohistochemical analysis, enzyme-linked immunosorbent assay and quantitative polymerase chain reaction were used to determine the therapeutic effects and molecular mechanism of butyrate treatment. The findings demonstrated that butyrate induced a marked shift in superoxide dismutase and catalase activities, along with a decrease in malondialdehyde levels, thereby attenuating oxidative stress. Furthermore, butyrate decreased the levels of pro-inflammatory cytokines interleukin-1β, tumour necrosis factor-α and leukotriene B4, which helped combat inflammatory responses. Moreover, butyrate treatment exerted remarkable positive influences that mediate an increase in 6-keto-PGF-1α (a degradation product of prostacyclin), trefoil factor 2, MUC5AC and fibroblast growth factor-7 levels to promote gastric mucosal repair. The expression of specific receptor GPR109A for butyrate was upregulated, with no significant difference noted in the expression of GPR43 or GPR41. Overall, the present findings revealed that butyrate exerted therapeutic effects by upregulating mucosal repair factors and stimulating protective responses against oxidation and inflammation. GPR109A may be the key receptor for butyrate therapy.

Proof-of-Principle Study Suggesting Potential Anti-Inflammatory Activity of Butyrate and Propionate in Periodontal Cells

“…On the other hand, in our study, butyrate was only effective in reducing CXCL1 and CXCL2 expression, while it was propionate that demonstrated attenuation of the IL1β- and TNFα-induced expression of IL8, CXCL1, and CXCL2 in HSC2 cells. Nevertheless, our data are consistent with findings that butyrate attenuates the excessive inflammation involved in the development of gastric mucosal ulcers induced by erosion due to acid in mice [ 54 ] and that butyrate inhibits LPS-induced cytokine production in mammary epithelial cells [ 55 ]. Butyrate further decreased TNFα-induced IL8 and CXCL2 expression in endothelial cells [ 56 , 57 ] and IL8 in the intestinal jejunal epithelial cell line J2 exposed to LPS [ 58 ].…”

Probiotic Supplementation With Saccharomyces boulardii and Enterococcus faecium Improves Gastric Pain and Bloating in Airline Pilots With Chronic Non-atrophic Gastritis: An Open-Label Study

“…One hypothesis is that S. boulardii can influence immunological function by enhancing the synthesis of short-chain fatty acids, including butyrate [23]. This is of interest as butyrate may aid in the repair of the gastric mucosa due to its anti-oxidative and anti-inflammatory properties [24]. In addition, animal studies have demonstrated that E. faecium may exert an immunomodulatory function [25].…”

Hypomagnetic Field Exposure Affecting Gut Microbiota, Reactive Oxygen Species Levels, and Colonic Cell Proliferation in Mice

“…Undigested carbohydrates are fermented by the gut microbiota into the SCFA acetate, propionate, and butyrate, which are beneficial to reducing inflammation, enhancing immunity and stimulating epithelial cell growth for the host [Macfarlane and Macfarlane, 2012]. Especially, SCFA butyrate has anti‐inflammatory and anti‐oxidative effects and improves gut barrier function, thus playing a role in oxidative stress in the healthy colonic mucosa [Hamer et al, 2009; Hamer et al, 2010; Zhou et al, 2021]. In this study, the trend of decreased butyrate in HMF‐exposed mice may attenuate its role in anti‐inflammatory and antioxidant effects in the colon.…”