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

BMC Complementary and Alternative Medicine

Ming Gao²  Lili Wu³  Liansha Huang¹  Xiangyu Guo³  Lingling Qin³  Wen Sun³  Boxin Zhou⁴  Tonghua Liu³  Hisae Yoshitomi²  Jingxin Zhou³ 

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

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

Others  :  1220278
DOI  :  10.1186/1472-6882-14-42

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

【 摘 要 】

Background

Isoquercitrin, 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.

Methods

To 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.

Results

Isoquercitrin 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.

Conclusions

Isoquercitrin 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】

   
2014 Zhou et al.; licensee BioMed Central Ltd.

【 图 表 】

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