Department of Anesthesiology, First Affliated Hospital of Anhui Medical University, Hefei 230022, China.
PPAR Res. 2012;2012:547980. doi: 10.1155/2012/547980. Epub 2011 Oct 9.
This study investigates the effects and possible mechanism of an agonist of PPARα, Wy14643, on primary hepatocytes subjected to H/R injury in rats. H/R induced a significant increase ALT, AST, MDA in the culture medium and ROS in the hepatocytes. These effects were reversed by pretreatment with Wy14643 in the dose-dependent manner. The activity of SOD and the level of GSH in the hepatocytes were decreased after H/R, which were increased by Wy14643 pretreatment. Moreover, the mRNA expressions of PPARα significantly increased in H/R+Wy14643 groups when compared with that in H/R group. A PPARα agonist, Wy14643, exerts significant protective effect against H/R injury in primary hepatocytes via PPARα activation and attenuating oxidative stress.
本研究探讨了过氧化物酶体增殖物激活受体α(PPARα)激动剂 Wy14643 对大鼠原代肝细胞缺氧/复氧(H/R)损伤的作用及可能机制。H/R 可导致培养基中 ALT、AST、MDA 显著增加,肝细胞内 ROS 显著增加,而 Wy14643 预处理呈剂量依赖性地逆转这些作用。H/R 后肝细胞中超氧化物歧化酶(SOD)活性和谷胱甘肽(GSH)水平降低,Wy14643 预处理可增加其水平。此外,与 H/R 组相比,H/R+Wy14643 组的 PPARα mRNA 表达显著增加。PPARα 激动剂 Wy14643 通过激活 PPARα 并减轻氧化应激对原代肝细胞的 H/R 损伤发挥显著的保护作用。