miR-34a 通过 ERK1/2 通路对急性心肌梗死大鼠心肌细胞凋亡的影响。
Influence of miR-34a on myocardial apoptosis in rats with acute myocardial infarction through the ERK1/2 pathway.
机构信息
Department of Cardiovascular Medicine, Linyi No. 3 People's Hospital, Linyi, China.
出版信息
Eur Rev Med Pharmacol Sci. 2019 Apr;23(7):3034-3041. doi: 10.26355/eurrev_201904_17585.
OBJECTIVE
To study the influence of micro-ribonucleic acid (miR)-34a on myocardial apoptosis in rats with acute myocardial infarction (AMI) through the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway.
MATERIALS AND METHODS
A total of 24 Sprague-Dawley (SD) rats were randomly divided into sham group (n=12) and model group (n=12). The heart was exposed in the sham group, while the AMI model was established in the model group. After sampling, the morphology of myocardial tissues was observed via hematoxylin-eosin (HE) staining, the expressions of B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) were detected via immunohistochemistry, and the protein expression levels of ERK1/2 and phosphorylated ERK1/2 (p-ERK1/2) were detected via Western blotting. Moreover, the expression of miR-34a was detected via quantitative Polymerase Chain Reaction (qPCR), the apoptosis was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), and the myocardial injury indexes were detected using a fully-automatic biochemical analyzer.
RESULTS
The morphology of myocardial tissues was normal with a complete structure in the sham group, while there was damage to myocardial tissues in different degrees in the model group. The immunohistochemical results revealed that the Bax expression was increased and the Bcl-2 expression was decreased in the model group compared with those in the sham group (p<0.05). The results of Western blotting showed that the protein expression levels of both ERK1/2 and p-ERK1/2 were significantly increased in the model group compared with those in the sham group (p<0.05). The qPCR results manifested that the expression of miR-34a in the model group markedly declined compared with that in the sham group (p<0.05). Besides, the TUNEL detection showed that the apoptosis rate in the model group was remarkably increased compared with that in the sham group (p<0.05), and the content of cardiac troponin T and creatine kinase isoenzyme in the model group was significantly higher than that in the sham group ((p<0.05).
CONCLUSIONS
MiR-34a affects the apoptosis in AMI by regulating the ERK1/2 signaling pathway.
目的
通过细胞外信号调节激酶 1/2（ERK1/2）通路研究微小 RNA-34a 对急性心肌梗死（AMI）大鼠心肌细胞凋亡的影响。
材料与方法
将 24 只 Sprague-Dawley（SD）大鼠随机分为假手术组（n=12）和模型组（n=12）。假手术组暴露心脏，模型组建立 AMI 模型。取样后，通过苏木精-伊红（HE）染色观察心肌组织形态，通过免疫组化检测 B 细胞淋巴瘤-2（Bcl-2）和 Bcl-2 相关 X 蛋白（Bax）的表达，通过 Western blot 检测 ERK1/2 和磷酸化 ERK1/2（p-ERK1/2）的蛋白表达水平。此外，通过实时定量聚合酶链反应（qPCR）检测 miR-34a 的表达，通过末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记（TUNEL）检测细胞凋亡，通过全自动生化分析仪检测心肌损伤指标。
结果
假手术组心肌组织形态正常，结构完整，模型组心肌组织损伤程度不同。免疫组化结果显示，与假手术组相比，模型组 Bax 表达增加，Bcl-2 表达减少（p<0.05）。Western blot 结果显示，与假手术组相比，模型组 ERK1/2 和 p-ERK1/2 的蛋白表达水平均显著升高（p<0.05）。qPCR 结果显示，与假手术组相比，模型组 miR-34a 的表达明显降低（p<0.05）。此外，TUNEL 检测显示，与假手术组相比，模型组细胞凋亡率明显升高（p<0.05），模型组肌钙蛋白 T 和肌酸激酶同工酶含量明显高于假手术组（p<0.05）。
结论
miR-34a 通过调节 ERK1/2 信号通路影响 AMI 中的细胞凋亡。
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