Proteomic study on the protective mechanism of fibroblast growth factor 21 to ischemia-reperfusion injury

被引：71

作者：

Cong, Wei-Tao ^{[1
]}

Ling, Jin ^{[1
,2
]}

Tian, Hai-Shan ^{[1
]}

Ling, Ren ^{[2
]}

Wang, Yang ^{[3
]}

Huang, Bin-Bin ^{[1
]}

Zhao, Ting ^{[1
]}

Duan, Yuan-Meng ^{[1
]}

Jin, Li-Tai ^{[1
]}

Li, Xiao Kun ^{[1
]}

机构：

[1] Wenzhou Med Coll, Zhejiang Prov Key Lab Biopharmaceut, Wenzhou 325035, Zhejiang, Peoples R China

[2] Jinhua Guangfu Tumour Hosp, Jinhua 321000, Zhejiang, Peoples R China

[3] Wenzhou Med Coll, Dept Histol & Embryol, Neurosci Inst, Wenzhou 325035, Zhejiang, Peoples R China

来源：

CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY | 2013年 / 91卷 / 11期

关键词：

FGF-21; myocardial ischemia-reperfusion; H9c2; proteomics; Akt; ROS; apoptosis; signaling pathway; PROTEIN-KINASE-C; ATP-SYNTHASE; ISCHEMIA/REPERFUSION INJURY; OXIDATIVE STRESS; CARDIAC-CELLS; HEAT-SHOCK; RAT-HEART; APOPTOSIS; CARDIOMYOPATHY; INACTIVATION;

D O I：

10.1139/cjpp-2012-0441

中图分类号：

R9 [药学];

学科分类号：

100702 [药剂学];

摘要：

Fibroblast growth factor (FGF)-21 is a novel regulator of insulin-independent glucose transport in 3T3-L1 adipocytes and has glucose and triglyceride lowering effects in rodent models of diabetes. In this study, we found that FGF-21 can significantly attenuate ischemia-reperfusion (I/R) induced damage in H9c2 cells (rat heart). However, it is unclear which signal transduction pathway is involved in the cardioprotective effect of FGF-21. Thus, this study was designed to investigate the potential mechanism induced by FGF-21. The results showed that FGF-21 treatment prevented the oxidative stress and apoptosis associated with I/R damage by reducing the levels of superoxide anions, inhibiting glycogen synthase kinase (GSK) 3 beta by activating Akt phosphorylation, and recovering the levels of ATP synthase pyruvate kinase isozymes M1 and protein kinase C, thereby improving energy supply. In summary, we conclude that FGF-21 protects H9c2 cells against I/R injury mainly through the Akt-GSK-3 beta-caspase-3 dependent pathway, preventing oxidative stress, and recovery of the energy supply.

引用

页码：973 / 984

页数：12

共 35 条

[1]

Noxa is necessary for hydrogen peroxide-induced caspase-dependent cell death [J].