RESUMO
@#【Objective】To explore miRNA-138 protecting cardiomyocyte apoptosis of neonatal rats by inhibiting JNK/ p38 MAPK pathway.【Methods】Thirty-three whole blood samples from patients with acute myocardial ischemia during the period from January 2018 to December 2018 were collected. Thirty- three whole blood samples from healthy people who underwent physical examination in the same period were enrolled as controls. Ischemia/reperfusion（I/R）models of neonatal rats were established. Forty neonatal rats were randomly divided into blank control group（Control），model group（I/R model），negative control group（injected with unordered sequence）and miRNA-138 overexpression group（Ad-miRNA-138），with 10 cases in each group. The expression of miRNA- 138，Bcl2 and Bax mRNA in whole blood and myocardial tissues was detected by qRT-PCR. The levels of rat hemodynamic indexes were detected by electrophysiological recorder. The pathological damages of myocardial tissues were observed by HE staining. The expression of Caspase- 3 in myocardial tissues was detected by immunohistochemistry. The apoptosis of myocardial cells was observed by TUNEL staining. The content of reactive oxygen species （ROS） in myocardial tissues was detected by ELISA. The expression of JNK/p38 MAPK pathway protein was detected by Western blotting. 【Results】 Compared with healthy control，the level of whole blood miRNA- 138 was significantly decreased in patients with acute myocardial ischemia（P<0.05）. Compared with I/R model group，cardiomyocyte gap in Ad-miRNA-138 group was smaller，its arrangement was more uniform，and its structure was more complete. The miRNA- 138 expression，levels of cardiac function indexes such as +dp/dtmax，HR，LVSP and Bcl2/Bax were significantly increased，while number of apoptosis cells，rate of Caspase-3 positive-expression cells， ROS，p-p38/p38，Pc-jun/c-jun and p-JNK1/2/JNK1/2 were significantly down-regulated（P<0.05）.【Conclusion】MiRNA- 138 can inhibit cardiomyocyte apoptosis of rats，and reduce ROS damage by inhibiting JNK/p38 MAPK pathway， thus protecting cardiomyocytes of neonatal rats.