Inhibition of uncoupling protein 2 with genipin exacerbates palmitate-induced hepatic steatosis

Lipids in Health and Disease

Research

Bing Tang¹  De Li¹  Dachun Yang¹  Shuangtao Ma¹  Yongjian Yang¹  Yan Tan¹ 

[1] Department of Cardiology, General Hospital of PLA Chengdu Military Area Command, 270 Rongdu Rd., Tianhui Town, 610083, Jinniu District, Chengdu, Sichuan Province, People’s Republic of China;

关键词: HepG2 Cell;    Palmitic Acid;    Hepatic Steatosis;    Nonalcoholic Fatty Liver Disease;    Genipin;   

DOI  :  10.1186/1476-511X-11-154

 received in 2012-05-10, accepted in 2012-11-06,  发布年份 2012

来源: Springer

【 摘 要 】

BackgroundUncoupling protein 2 (UCP2) was reported to be involved in lipid metabolism through regulating the production of superoxide anion. However, the role of UCP2 in hepatocytes steatosis has not been determined. We hypothesized that UCP2 might regulate hepatic steatosis via suppressing oxidative stress.ResultsWe tested this hypothesis in an in vitro model of hepatocytic steatosis in HepG2 cell lines induced by palmitic acid (PA). We found that treatment with PA induced an obvious lipid accumulation in HepG2 cells and a significant increase in intracellular triglyceride content. Moreover, the specific inhibition of UCP2 by genipin remarkably exacerbated PA-induced hepatocytes steatosis. Interestingly, the PA-induced superoxide overproduction can also be enhanced by incubation with genipin. In addition, administration with the antioxidant tempol abolished genipin-induced increase in intracellular lipid deposition. We further found that genipin significantly increased the protein expression of fatty acid translocase (FAT)/CD36.ConclusionsThese findings suggest that UCP2 plays a protective role in PA-induced hepatocytic steatosis through ameliorating oxidative stress.

【 授权许可】

Unknown   
© Ma et al.; licensee BioMed Central Ltd. 2012. 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 cited.