Plant sterol ester of α-linolenic acid improves NAFLD through modulating gut microbiota and attenuating lipopolysaccharide-induced inflammation via regulating TLR4/NF-κB signaling pathway. (July 2022)

• Record Type: Journal Article
• Authors: Han, Hao; Wang, Linqi; Xue, Tingli; Li, Jie; Pei, Liyuan; Zheng, Mingming
• Is Part Of: Journal of functional foods. Volume 94(2022)
• Publication Date: 2022-07
• Subjects: Plant sterol ester of α-linolenic acid -- Gut microbiota -- Nonalcoholic fatty liver disease -- Lipopolysaccharide -- TLR4; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2022.105137
• Languages: English
• ISSNs: 1756-4646

Abstract

Graphical abstract: Highlights: PS-ALA treatment mitigates inflammation in the liver and prevents NAFLD. PS-ALA modulates gut microbiota and maintains intestinal barrier function. PS-ALA reduces LPS production and attenuates LPS-triggered hepatic inflammation. PS-ALA inhibits LPS-triggered TLR4/NF-κB signaling pathway activation. Abstract: Lipopolysaccharide (LPS) originating from dysbiotic gut microbiota is regarded as a critical mediator for triggering the inflammation responsible for non-alcoholic fatty liver disease (NAFLD). The preventive effect of plant sterol ester of α-linolenic acid (PS-ALA) on NAFLD was identified in our previous research, yet, the mechanisms linking this effect to gut microbiota and LPS-triggered inflammation remain unclear. In present study, we found that PS-ALA treatment could counteract gut microbial dysbiosis and maintain intestinal barrier function. These beneficial effects of PS-ALA reduced bacterial LPS production and leakage into the portal circulation which attenuated LPS-triggered hepatic inflammation. In addition, PS-ALA inhibited LPS-triggered TLR4/NF-κB signaling pathway activation and reduced pro-inflammatory cytokines release in HepG2 cells. In conclusion, PS-ALA has a dual inhibition effect on endotoxin, including reducing LPS production in the gut and blocking the activation of the LPS-induced TLR4/NF-κB signaling pathway, thereby mitigating inflammatory reactions in the liver and preventing NAFLD.