Lipotoxic Effect of p21 on Free Fatty Acid-Induced Steatosis in L02 Cells

被引：4

作者：

Wang, Jie-wei ^{[1
]}

Wan, Xing-yong ^{[1
]}

Zhu, Hua-tuo ^{[1
]}

Lu, Chao ^{[1
]}

Yu, Wei-lai ^{[1
]}

Yu, Chao-hui ^{[1
]}

Shen, Zhe ^{[1
]}

Li, You-ming ^{[1
]}

机构：

[1] Zhejiang Univ, Coll Med, Affiliated Hosp 1, Dept Gastroenterol, Hangzhou 310003, Zhejiang, Peoples R China

来源：

PLOS ONE | 2014年 / 9卷 / 04期

基金：

中国国家自然科学基金;

关键词：

LIVER-DISEASE; NONALCOHOLIC STEATOHEPATITIS; PROTEASOME INHIBITOR; OXIDATIVE STRESS; PROGRESSION; MICE; SENESCENCE; REGENERATION; PATHOGENESIS; HEPATOCYTES;

D O I：

10.1371/journal.pone.0096124

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Nonalcoholic fatty liver disease (NAFLD) is increasingly regarded as a hepatic manifestation of metabolic syndrome. Though with high prevalence, the mechanism is poorly understood. This study aimed to investigate the effects of p21 on free fatty acid (FFA)-induced steatosis in L02 cells. We therefore analyzed the L02 cells with MG132 and siRNA treatment for different expression of p21 related to lipid accumulation and lipotoxicity. Cellular total lipid was stained by Oil Red O, while triglyceride content, cytotoxicity assays, lipid peroxidation markers and anti-oxidation levels were measured by enzymatic kits. Treatment with 1 mM FFA for 48 hr induced magnificent intracellular lipid accumulation and increased oxidative stress in p21 overload L02 cells compared to that in p21 knockdown L02 cells. By increasing oxidative stress and peroxidation, p21 accelerates FFA-induced lipotoxic effect in L02 cells and might provide information about potentially new targets for drug development and treatments of NAFLD.

引用

页数：8

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