青藤碱抑制H2O2诱导乳鼠心肌细胞凋亡

Inhibitory effect of sinomenine on H_2O_2-induced apoptosis in neonatal rat cardiomyocytes

目的:探讨青藤碱对H2O2诱导乳鼠心肌细胞凋亡的影响及其可能的作用机制。方法:在原代培养的SD大鼠乳鼠心肌细胞上建立H2O2损伤模型,观察不同剂量青藤碱(10,30,100μmol.L-1)对心肌细胞凋亡率、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性、乳酸脱氢酶(LDH)活性及NF-κB蛋白表达的影响。结果:H2O2组与空白对照组相比,心肌细胞凋亡率显著增加(P<0.01),并随着时间的延长其凋亡率不断增高;青藤碱明显抑制H2O2所诱导各个时间段的心肌细胞凋亡率(P<0.01),降低MDA含量,增加SOD,LDH活性,抑制NF-κB蛋白表达。结论:青藤碱对H2O2诱导的乳鼠心肌细胞凋亡有抑制作用,其作用机制可能与其抗脂质氧化、抑制心肌细胞表达NF-κB有关。

Objective： To study the effects of sinomenine on apoptosis in cutured neonatal rat cardiomyocytes induced by H2O2 and its possible mechanism. Method： H2O2 was used to build an oxidative stress-induced injury model in neonatal rat cardiomyocytes after being treated with sinomenine （ 10, 30, 100 μmol · L^-1 ）, the apoptosis rate, the content of malondialdehyde （ MDA）, the activ- ity of superoxide dimutase （SOD）, the activity of lactate dehydrogenase （LDH） and expression of NF-κB protein of the Cardiomyocytes were examined. Result： Compared with the model group, the apoptosis rate and the content of MDA, LDH decreased greatly （P 〈 0. 01 ）, and the activity of SOD increased distinctly （ P 〈0.01 ） after being treated by sinomenine （ 10, 30, 100 μmol · L^-1 ）. Conclusion： Sinomenine can inhibit the apoptosis induced by H2O2 in neonatal rat cardiomyocytes. The protective mechanism could be related to its ability to reduce lipid pexosidation and to inhibit cardiomyocyte expression of NF-κB protein.