Quercetin ameliorates lipid deposition in primary hepatocytes of the chicken embryo

文献类型： 外文期刊

第一作者： Feng, Y.

作者： Feng, Y.;Zhao, C.;Li, T.;Wang, M.;Zhao, W.;Shen, M.;Serrano, B. R.;Barcenas, A. R.;Zhao, W.;Qu, L.;Shen, M.

作者机构：

关键词： Quercetin; chicken; fatty liver; SREBP-1; AKT; ERK

期刊名称：BRITISH POULTRY SCIENCE （ 影响因子：2.0； 五年影响因子：2.2 ）

ISSN： 0007-1668

年卷期： 2024 年

页码：

收录情况： SCI

摘要： 1. The accumulation of excessive fat plays a role in the development of non-alcoholic fatty liver disease (NAFLD) and phytogenic feed additives have the potential to ameliorate this. This study involved the isolation and culture of primary hepatocytes from chicken embryos to establish a model of hepatic steatosis induced by oleic acid/dexamethasone (OA/DEX). Lipid accumulation and cell viability were assessed using Nile Red staining, Oil Red O staining and cell count Kit -8 (CCK8) following treatment with varying concentrations of quercetin (Que). The potential mechanism by which Que exerts its effects was preliminarily investigated.2. The results indicated that OA effectively treated lipid accumulation in hepatocytes. There was no notable variance in cell proliferation between the normal and OA/DEX groups when subjected to Que treatment at concentrations of 1000 ng/ml and 10 000 ng/ml. Triglycerides and cholesterol (low and high density) decreased with Que treatment, with the most substantial reduction observed at 10 000 ng/ml.3. Gene expression levels decreased to levels similar to those in the control groups. Western blot data demonstrated that sterol regulatory element-binding protein 1 (SREBP-1) protein expression correlated with its mRNA expression level. Que mitigated lipid accumulation through the alpha serine/threonine protein kinase (AKT) and extracellular signal-regulated kinase (ERK) pathways. Expression levels of lipid-related genes (APOB, PPAR alpha, CYP3A5 and SREBP-1) decreased to levels similar to the control groups. Western blot data demonstrated that the SREBP-1 protein expression correlated with its mRNA expression level.4. Supplementation with Que ameliorated lipid accumulation through AKT and ERK signalling pathway in OA/DEX-induced high-fat hepatocytes.

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