Antiapoptotic effect of glutaredoxin in cardiomyocytes by inducing changes in the cellular redox system.

已知谷氧还蛋白（GRX）通过调节某些蛋白质的氧化还原状态来保护细胞免受氧化应激。在GRX 1过表达的大鼠心肌H9 c2细胞（H9 c2-GRX）中，与H9 c2对照细胞（H9 c2-control）相比，一氧化氮（NO）诱导的凋亡和甘油醛-3-磷酸脱氢酶（GAPDH）活性的降低被抑制。此外，在NO刺激下，H9 c2-GRX中GAPDH的核转位和蛋白质的S-亚硝基化与H9 c2-对照相比受到抑制。这些数据表明，GRX 1的过表达可以保护心肌细胞免受NO诱导的凋亡，可能通过抑制氧化修饰和GAPDH的核转位。

It is known that glutaredoxin (GRX) protects cells from oxidative stress by regulating the redox state of certain proteins. In GRX1-overexpressed rat myocardiac H9c2 cells (H9c2-GRX), nitric oxide (NO)-induced apoptosis and decreasing of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity was suppressed compare to H9c2-control cells (H9c2-control). Furthermore, under NO stimulation, nuclear translocation of GAPDH and S-nitrosylation of protein was suppressed in H9c2-GRX compare to H9c2-control. These data suggest that the overexpression of GRX1 could protect cardiomyocytes against NO-induced apoptosis, likely through the inhibition of the oxidative modification and the nuclear translocation of GAPDH.