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沙术醇和槲皮素对吉富罗非鱼肝脂肪变性原代细胞脂滴蓄积的调控机制

Regulatory mechanism of Sarmentosin and Quercetin on lipid accumulation in primary hepatocyte of GIFT tilapia (Oreochromis niloticus) with fatty liver.

机构信息

College of Animal Science and Technology, Guangxi University, Nanning, China.

出版信息

PLoS One. 2024 Sep 5;19(9):e0309976. doi: 10.1371/journal.pone.0309976. eCollection 2024.

DOI:10.1371/journal.pone.0309976
PMID:39236049
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11376590/
Abstract

Sarmentosin (SA) and Quercetin (QC) are two active components of Sedum Sarmentosum Bunge, which is a traditional Chinese herbal medicine. This study aimed to investigate the role and regulatory mechanism of SA and QC in fatty liver of Genetic Improvement of Farmed Tilapia (GIFT) tilapia. GIFT tilapia were randomly divided into two groups with three replicates per treatment (30 fish in each replicate): normal diet group (average weight 3.51±0.31 g) and high-fat diet group (average weight 3.44±0.09 g). After 8 weeks feeding trial, growth index, lipid deposition, and biochemical indexes were measured. Lipid deposition, and lipid and inflammation-related gene expression were detected in a primary hepatocyte model of fatty liver of GIFT tilapia treated with SA or QC. Our results showed that high-fat diet caused lipid deposition and peroxidative damage in the liver of GIFT tilapia. The cell counting kit-8 assay results indicated that 10 μM SA and 10 μM of QC both had the least effect on hepatocyte proliferation. Moreover, both 10 μM of SA and 10 μM of QC showed lipolytic effects and inhibited the expression of lipid-related genes (FAS, Leptin, SREBP-1c, and SREBP2) in fatty liver cells. Interestingly, QC induced autophagosome-like subcellular structure and increased the expression of IL-8 in fatty liver cells. In conclusion, this study confirmed that SA and QC improved fatty liver caused by high-fat diet, providing a novel therapeutic approach for fatty liver of GIFT tilapia.

摘要

三叶香茶菜素(SA)和槲皮素(QC)是传统中药三叶香茶菜的两种活性成分。本研究旨在探讨 SA 和 QC 在吉富罗非鱼脂肪肝中的作用及其调控机制。将吉富罗非鱼随机分为两组,每组三个重复(每个重复 30 条鱼):正常饮食组(平均体重 3.51±0.31 g)和高脂饮食组(平均体重 3.44±0.09 g)。经过 8 周的饲养试验,测量生长指标、脂质沉积和生化指标。在吉富罗非鱼脂肪肝原代肝细胞模型中,用 SA 或 QC 处理后检测脂质沉积以及脂质和炎症相关基因的表达。我们的结果表明,高脂饮食导致吉富罗非鱼肝脂质沉积和过氧化损伤。细胞计数试剂盒-8 检测结果表明,10 μM 的 SA 和 10 μM 的 QC 对肝细胞增殖的影响最小。此外,10 μM 的 SA 和 10 μM 的 QC 均具有脂肪分解作用,并抑制脂肪肝细胞中脂质相关基因(FAS、瘦素、SREBP-1c 和 SREBP2)的表达。有趣的是,QC 诱导自噬体样亚细胞结构,并增加脂肪肝细胞中 IL-8 的表达。总之,本研究证实了 SA 和 QC 改善了高脂饮食引起的脂肪肝,为吉富罗非鱼脂肪肝提供了一种新的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7eb/11376590/eb55db4e38b3/pone.0309976.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7eb/11376590/5aaf755ec7c0/pone.0309976.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7eb/11376590/eb55db4e38b3/pone.0309976.g005.jpg
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