Isoquercitrin activates the AMP–activated protein kinase (AMPK) signal pathway in rat H4IIE cells

BMC Complementary and Alternative Medicine

Research Article

Wen Sun¹  Xiangyu Guo¹  Lili Wu¹  Tonghua Liu¹  Jingxin Zhou¹  Lingling Qin¹  Boxin Zhou²  Hisae Yoshitomi³  Ming Gao³  Liansha Huang⁴ 

[1] Beijing University of Chinese Medicine, 11 North 3rd-ring East Road, 100029, Beijing, Chaoyang District, People’s Republic of China;Sanshui Hospital affiliated to Guangdong Medical college, 16 Guanghai West Road, 528000, Foshan, Guangdong, People’s Republic of China;School of Pharmaceutical Sciences, Mukogawa Women’s University, 11-68 Koshien Kyuban-cho, 663-8179, Nishinomiya, Hyogo, Japan;Shenzhen TCM Hospital, 1 Fuhua Road, Shenzhen, 518000, Guangdong, Futian District, People’s Republic of China;

关键词: Isoquercitrin;    H4IIE cells;    AMPK;    AdipoR1;   

DOI  :  10.1186/1472-6882-14-42

 received in 2013-08-20, accepted in 2014-01-31,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundIsoquercitrin, a flavonoid compound that is widely distributed in medicinal and dietary plants, possesses many biological activities, including inhibition of adipocyte differentiation. In this study, we investigated the effect of isoquercitrin on lipid accumulation and its molecular mechanisms in rat hepatoma H4IIE cells.MethodsTo investigate the effect of isoquercitrin on lipid accumulation, H4IIE cells were induced by FFA and the total lipid levels were detected by Oil Red O staining. Furthermore, The protein levels of AMPK and acetyl-CoA carboxylase (ACC), the gene expressions of transcriptional factor, lipogenic genes, and adiponectin receptor 1 (AdipoR1) were analyzed by Western blotting and quantitative real-time PCR. To further confirm the pathway of isoquercitrin-mediated hepatic lipid metabolism, H4IIE cells were treated with an AMPK inhibitor and AdipoR1 siRNA.ResultsIsoquercitrin significantly enhances AMPK phosphorylation, downregulates sterol regulatory element binding protein transcription factor 1 (SREBP-1) and fatty acid synthase (FAS) gene expressions. Pretreatment with AMPK inhibitor, significantly decreased the AMPK phosphorylation and increased FAS expression stimulated by isoquercitrin. Isoquercitrin might also upregulate the expression of AdipoR1 dose-dependently via AMPK in the presence of an AMPK inhibitor and AdipoR1 siRNA.ConclusionsIsoquercitrin appears to regulate AMPK activation, thereby enhancing AdipoR1 expression, suppressing SREBP-1 and FAS expressions, and resulting in the regulation of lipid accumulation. These results suggest that isoquercitrin is a novel dietary compound that can be potentially be used to prevent lipid metabolic disorder and nonalcoholic fatty liver disease.

【 授权许可】

Unknown   
© Zhou et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited.