微小RNA-199a-3p靶向非受体酪氨酸激酶信号转导和转录激活因子3对心力衰竭的影响  

Effect of miR-199a-3p targeting JAK signal transduction and STAT3 pathway on cardiac funtion in rat HF model

作　　者：张士锋[1] 李永格[1] 魏浩[1] 王海洋[2] 高建步[2] 冯怡锟[3] Zhang Shifeng;Li Yongge;Wei Hao;Wang Haiyang;Gao Jianbu;Feng Yikun(Department of Basic Medical Sciences,Nanyang Higher Medical Training School,Nanynag 473000,Henan Province,China)

机构地区：[1]南阳医学高等专科学校基础医学部,473000 [2]南阳市中心医院心血管内科一病区 [3]郑州大学第二附属医院病理科

出　　处：《中华老年心脑血管病杂志》2022年第3期311-314,共4页Chinese Journal of Geriatric Heart,Brain and Vessel Diseases

基　　金：河南省科技发展计划项目(212102310837)。

摘　　要：目的探究微小RNA(miR)-199a-3p调控非受体酪氨酸激酶(JAK)信号转导和转录激活因子3(STAT3)通路对心力衰竭(HF)大鼠模型心脏功能的影响和机制。方法30只建模成功的大鼠随机分为HF+miR-199a-3p组和HF组(n=15),选取15只正常大鼠作为对照组。HF+miR-199a-3p组尾静脉注射miR-199a-3p类似物。检测各组miR-199a-3p、心肌细胞凋亡指数、炎性因子白细胞介素6(IL-6)、TNF-α、JAK和STAT3蛋白表达水平。结果HF组miR-199a-3p表达明显低于对照组,心肌细胞凋亡指数、IL-6、TNF-α、JAK及STAT3蛋白表达明显高于对照组(P<0.05)。HF+miR-199a-3p组miR-199a-3p明显高于HF组,心肌细胞凋亡指数、IL-6、TNF-α、JAK2和STAT3蛋白水平明显低于HF组,有统计学差异[1.67±0.11 vs 0.41±0.05,(13.62±1.47)%vs(28.34±2.75)%,(26.73±3.17)ng/L vs(38.21±4.09)ng/L,(25.56±2.98)ng/L vs(47.24±5.11)ng/L,1.82±0.16 vs 3.65±0.31,2.04±0.17 vs 3.89±0.33,P<0.05]。结论miR-199a-3p通过抑制JAK/STAT通路缓解炎性反应抑制心肌细胞的凋亡,从而提高HF大鼠心功能。Objective To study the effect of miR-199a-3p-regulated JAK signal transduction and STAT3 pathway on cardiac funtion in rat HF model and its mechanism.Methods Thirty rats were randomly divided into HF+miR-199a-3p group(n=15)and HF group(n=15)with 15 healthy rats served as a control group.MiR-199a-3p mimic was injected into the animals through their tail vein.The expressions of miR-199a-3p,IL-6,TNF-α,JAK and STAT3 protein,and cardiomyocyte apoptosis index in different groups were detected.Results The serum miR-199a-3p level was significantly lower while the cardiomyocte apoptosis index and expression levels of IL-6,TNF-α,JAK and STAT3 protein were significantly higher in HF group than in control group(P<0.05).The serum miR-199a-3p level was significantly higher while the cardiomyocte apoptosis index and expression levels of IL-6,TNF-α,JAK and STAT3 protein were significantly lower in HF+miR-199a-3p group than in HF group(1.67±0.11 vs 0.41±0.05,13.62%±1.47%vs 28.34%±2.75%,26.73±3.17 ng/L vs 38.21±4.09 ng/L,25.56±2.98 ng/L vs 47.24±5.11 ng/L,1.82±0.16 vs 3.65±0.31,2.04±0.17 vs 3.89±0.33,P<0.05).Conclusion miR-199a-3p supresses the apoptosis of cardiomyocytes by inhibiting the JAK/STAT pathway,which can thus alleviate the inflammatory response and improve the cardiac function of HF rats.

关 键 词：微RNAS 细胞凋亡 转录激活因子3 心力衰竭 

分 类 号：R541.6[医药卫生—心血管疾病]