大株红景天对心肌细胞缺糖缺氧损伤的作用及机制研究

Protective effects and mechanism of Dazhuhongjingtian on OGD/R induced injury in H9c2 cells

目的:研究大株红景天对心肌细胞缺糖缺氧(OGD/R)损伤的保护作用及机制,探讨其与Akt/Nrf2信号通路的关系。方法:以大株红景天对氧化损伤心肌细胞存活率、乳酸脱氢酶(LDH)漏出率、丙二醛(MDA)含量、一氧化氮(NO)含量、超氧化物歧化酶(SOD)活力的影响为评价指标,研究大株红景天对OGD/R心肌细胞的保护作用,利用PI3K抑制剂联合药物处理细胞,Western blot法检测细胞中p-Akt、Akt、Nrf-2、HO-1蛋白的表达。结果:与模型组相比,大株红景天100μg/ml组能明显降低OGD/R损伤心肌细胞LDH漏出、MDA含量、NO含量,显著升高SOD活性和细胞存活率,同时上调缺糖缺氧诱导的p-Akt、Nrf-2、HO-1蛋白表达的升高,并能够被PI3K信号通路抑制剂抑制。结论:大株红景天对OGD/R损伤的H9C2细胞损伤具有显著的抑制作用,其作用机制可能与激活Akt/Nrf2信号通路有关。

Objective: To investigate the effect of Dazhuhongjingtian( DZHJT) on oxidative stress induced by OGD/reoxygenation in H9 c2 myocardial cell and explore the underlying mechanisms. Methods: The effects of DZHJT were evaluated in terms of the cell viability,the release of lactate dehydrogenase( LDH),the concentrations of nitric oxide( NO),malondialdehyde( MDA) and superoxide dismutase( SOD). After pretreated with PI3 K inhibitors,Western blotting was used to detect protein levels of hemeoxygenase-1( HO-1),protein kinase B( Akt),nuclear factor-like2( Nrf2) and phosphorylated Akt( p-Akt). Results: The results showed that DZHJT( 100μg/ml) significantly increased the cell viability and SOD level,suppressed the releases of LDH,NO,MDA and up-regulated the expressions of p-Akt,Nrf2 and HO-1 in cells induced by OGD/R injury. DZHJT combined with LY294002 resulted in a inhibition of the protein levels of p-AKT,Nrf2 and HO-1.Conclusion: The results suggest that DZHJT can inhibit oxidative stress injury induced by OGD,and its mechanism may be associated with activating the Akt/Nrf2 signaling pathway.