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Berberine alleviates hepatic lipid accumulation by increasing ABCA1 through the protein kinase C δ pathway.

Abstract：

:Abnormal lipid metabolism may contribute to the pathogenesis of non-alcoholic steatohepatitis (NASH). The ATP-binding cassette transporter A1 (ABCA1) protein mediates the transport of cholesterol and phospholipids from cells to apolipoprotein A-I (apoA-I) to generate nascent HDL particles. Previous studies revealed that the overexpression of ABCA1 alleviated hepatic lipid levels by modifying lipid transport. Here, we examined the effect of berberine (BBR) on ABCA1 in QSG-7701 hepatocytes and in mice. BBR decreased hepatic cholesterol and triglyceride levels. It also increased ABCA1 protein levels but not mRNA levels in a time- and dose-dependent manner. The PKCδ inhibitor rottlerin and PKCδ siRNA completely abolished the effect of BBR on ABCA1. BBR also decreased the phosphorylation of ABCA1 serine residues and PKCδ Tyr 311. The inhibition of ABCA1 with its siRNA abolished the reduction in cellular cholesterol levels by BBR. BBR administration to mice fed a methionine choline-deficient diet also significantly increased ABCA1 protein levels and reduced hepatic lipid levels. These results suggest that BBR can reduce steatosis by increasing ABCA1 protein levels through PKCδ to reduce the phosphorylation of serine residues in ABCA1.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Liang H,Wang Y

doi

10.1016/j.bbrc.2018.03.003

subject

Has Abstract

pub_date

2018-04-06 00:00:00

pages

473-480

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(18)30470-4

journal_volume

498

pub_type

杂志文章

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