心衰合剂对肥大心肌细胞线粒体MAO、COX活性的影响

Effect of Xinshuai mixture on MAO and COX activity in hypertrophy myocardial cell

目的通过大鼠原代心肌细胞培养,探讨心衰合剂对肥大心肌细胞线粒体功能的影响。方法培养大鼠原代心肌细胞,应用血管紧张素II(Ang II)造模,采用ELISA法检测心肌细胞超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(methane dicarboxylic aldehyde,MDA)、单胺氧化酶(monoamine oxidase,MAO)及环氧化酶(cyclooxygenase,COX)活性水平,反映线粒体功能及氧化应激损伤情况;Real-time PCR法检测细胞中caspase-3的表达水平。结果造模后,模型组心肌细胞SOD显著降低,MDA上升,MAO活性升高,COX活性降低,caspase-3 mRNA表达水平显著增加(P<0.01)。含药血清组及空白血清组SOD较模型组均有升高,MDA下降,但含药血清组SOD较空白血清组升高,MAO活性降低,COX活性升高(P<0.05,P<0.01);含药血清干预后,细胞内caspase-3 mRNA含量与模型组相比显著降低(P<0.01)。含药血清组caspase-3 mRNA表达显著低于空白血清组(P<0.01)。结论心衰合剂含药血清干预肥大心肌细胞可以显著改善线粒体功能,减轻能量代谢损伤及氧化应激损伤,并通过降低caspase-3的表达水平减轻细胞凋亡,保护心肌细胞。

Objective To study the effects of Xinshuai mixture on mitochondrial function of hypertrophy cardiomyocyte cell in vitro. Methods The primary neonatal rat myocardial cells were cultured to establish hypertrophic myocardial model by Ang II. The levels of superoxide dismutase（SOD）,methane dicarboxylic aldehyde（MDA）,monoamine oxidase（MAO） and cyclooxygenase（COX） were detected by ELISA,as the mitochondrial function and oxidative stress damage. The expression level of caspase-3 mRNA was detected by Real-time PCR. Results Compared with control group,the SOD level in model group reduced markedly,MDA level increased significantly,the activities of MAO increased,the activities of COX decreased,the expression of caspase-3 level increased significantly（P〈0. 01）. Compared with the model group,the SOD level increased and MDA level decreased in Xinshuai mixture group and blank serum group. But the SOD level and activities of MAO,COX in Xinshuai mixture group and blank serum group had significant difference（P〈0. 05,P〈0. 01）. The expression of caspase-3 mRNA level in Xinshuai mixture was significantly higher than the blank serum group（P〈0. 01）. Conclusion Xinshuai mixture could significantly improve the fuction of mitochondrial in hypertrophy cardiomyocyte cell,reduce the energy metabolism and oxidative stress injury,and protect cardiac myocyte through lower the expression of caspase-3.