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的伤害。在GRX1过表达的大鼠心肌H9c2细胞(H9c2-GRX)中，与H9c2对照细胞(H9c2-对照)相比，一氧化氮(NO)诱导的细胞凋亡和3-磷酸甘油醛脱氢酶(GAPDH)活性的下降受到抑制。此外，在没有刺激的情况下，H9c2-GRX组的GAPDH核转位和蛋白质的S亚硝化反应比H9c2-对照组受到抑制。这些结果表明，GRX1的过表达可能通过抑制GAPDH的氧化修饰和核转位来保护心肌细胞免受NO诱导的细胞凋亡。

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.