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Taxifolin ameliorate high-fat-diet feeding plus acute ethanol binge-induced steatohepatitis through inhibiting inflammatory caspase-1-dependent pyroptosis. | LitMetric

Taxifolin ameliorate high-fat-diet feeding plus acute ethanol binge-induced steatohepatitis through inhibiting inflammatory caspase-1-dependent pyroptosis.

Food Funct

Key Laboratory of Natural Medicines of the Changbai Mountain, Ministry of Education, College of Pharmacy, Yanbian University, Yanji, Jilin Province 133002, China. and Key Laboratory for Traditional Chinese Korean Medicine of Jilin Province, College of Pharmacy, Yanbian University, Yanji, Jilin Province 133002, China.

Published: January 2021

AI Article Synopsis

  • Excessive alcohol consumption combined with a high-fat diet can lead to steatohepatitis, presenting a serious health issue related to both alcoholic liver disease (AFLD) and non-alcoholic fatty liver disease (NAFLD).
  • Taxifolin (TAX), a natural compound derived from plants, has been identified to regulate lipid synthesis by inhibiting certain proteins and reducing inflammation in liver cells impacted by these dietary factors.
  • The study suggests TAX may serve as a potential treatment for steatohepatitis and non-alcoholic fatty liver degeneration by targeting specific inflammatory processes and preventing harmful cell death related to caspase-1 activation.

Article Abstract

Excessive alcohol drinking and a high-fat diet (HFD) promote steatohepatitis in the comorbidity of NAFLD and AFLD. Taxifolin (TAX) is a rich dihydroxyflavone compound found in onions, milk thistle and Douglas fir. We aimed to explore the intervention mechanism of TAX on chronic steatohepatitis induced by HFD feeding plus acute ethanol binge. We established an in vivo model by HFD feeding plus a single dose of ethanol binge, and established an in vitro model by oleic acid or palmitic acid on HepG2 cells to induce lipid accumulation. TAX regulated lipid synthesis by inhibiting the expression of SREBP1 and upregulating the PPARγ level. In addition, TAX inhibited the expression of P2X7R, IL-1β, and caspase-1. Moreover, TAX reduced the expression of caspase-1 activation; thereby inhibiting the recruitment of macrophages and neutrophils. TAX also improved the inflammatory response caused by caspase-1 activation in steatotic hepatocytes. TAX exhibited an inhibitory effect on lipid accumulation and caspase-1-related pyroptosis. Collectively, TAX has therapeutic potential as an intervention of steatohepatitis induced by alcohol combined with HFD and for preventing non-alcoholic fatty liver degeneration targeting caspase-1-dependent pyroptosis.

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Source
http://dx.doi.org/10.1039/d0fo02653kDOI Listing

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