五味子乙素对心肌细胞的氧化应激损伤的保护作用及其机制

Protective Effect and Mechanism of Schisandrin B on Oxidative Stress Injury in Cardiac Myocyte

研究了五味子乙素(Schisandrin B,SchB)对过氧化氢(H2O2)诱导小鼠原代心肌细胞体外氧化应激损伤的保护作用,并对其作用机制进行探讨。结果发现:与对照组相比,H2O2诱导组中心肌细胞的增殖明显受到抑制,氧化损伤产物丙二醛(MDA)和一氧化氮(NO)、促氧化蛋白p67-phox和p47-phox以及信号通路蛋白Trfa6和p-TAK1水平显著升高,而超氧化物歧化酶(SOD)及抗氧化蛋白HO-1水平显著降低,差异均有统计学意义(p<0. 01);与H2O2诱导组相比,SchB诱导心肌细胞增殖呈现浓度依赖性,显著抑制MDA、NO、p67-phox、p47-phox、Trfa6及p-TAK1的表达,显著诱导SOD和HO-1的表达,差异均有统计学意义(p<0. 05)。研究表明,SchB增强心肌细胞的抗氧化能力与抑制Traf6/TAK1信号传导有关。

The protective effect of Schisandrin B(SchB) on oxidative stress induced by H2O2 in cardiac myocytes and its potential mechanism were studied in vitro. The results show that compared with control group, the survival rates of cardiac myocyte, the levels of MDA, NO, p67-phox, p47-phox, Traf6 and p-TAK1 are significantly increased while the levels of SOD and HO-1 are greatly decreased(p<0.01). Compared with H2O2-induced group, the survival rates of cardiac myocyte, the levels of MDA, NO,p67-phox, p47-phox, Traf6 and p-TAK1 are significantly decreased while the levels of SOD and HO-1 are greatly increased with a concentration-dependent manner(p<0.05). It is concluded that SchB can inhibit the oxidative stress injury in cardiac myocyte partially via suppressing the activation of Traf6/TAK1 signaling pathway.