Oxidative stress results in myocardial cell apoptosis and even life-threatening heart failure in myocardial ischemia-reperfusion injury. Specific blocking of the complex I could reduce cell apoptosis. Ndufs4 is a nuclear-encoded subunit of the mitochondrial complex I and participates in the electron transport chain. In this study, we designed and synthesized siRNA sequences knocking down the rat Ndufs4 gene, constructed recombinant adenovirus Ndufs4 siRNA (Ad-Ndufs4 siRNA), and primarily verified the role of Ndufs4 in oxidative stress injury. The results showed that the adenovirus infection rate was about 90%, and Ndufs4 mRNA and protein were decreased by 76.7% and 64.9%, respectively. Furthermore, the flow cytometry assay indicated that the cell apoptosis rate of the Ndufs4 siRNA group was significantly decreased as compared with the H₂O₂-treated group. In conclusion, we successfully constructed Ndufs4 siRNA recombinant adenovirus; furthermore, the downexpression of the Ndufs4 gene may alleviate H₂O₂-induced H9c2 cell apoptosis.

中文翻译：

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重组腺病毒siRNA敲低Ndufs4基因减轻氧化应激损伤诱导的心肌细胞凋亡

氧化应激导致心肌细胞凋亡，在心肌缺血再灌注损伤中甚至危及生命的心力衰竭。特异性阻断复合物 I 可以减少细胞凋亡。Ndufs4 是线粒体复合体 I 的核编码亚基，参与电子传递链。本研究设计合成了敲低大鼠Ndufs4基因的siRNA序列，构建了重组腺病毒Ndufs4 siRNA（Ad-Ndufs4 siRNA），初步验证了Ndufs4在氧化应激损伤中的作用。结果表明，腺病毒感染率约为90%，Ndufs4 mRNA和蛋白分别降低76.7%和64.9%。此外，流式细胞术检测表明，与H相比，Ndufs4 siRNA组的细胞凋亡率显着降低₂ O ₂处理组。综上所述，我们成功构建了Ndufs4 siRNA重组腺病毒；此外，下调Ndufs4基因可减轻H ₂ O ₂诱导的H9c2细胞凋亡。