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目的 探讨miR-150-5p在小鼠心肌缺血再灌注损伤(MIRI)中作用机制，评估其对心肌损伤的保护作用及潜在的调控途径。方法 体外实验中，通过缺氧/复氧(H/R)处理H9c2心肌细胞，模拟MIRI模型。将H9c2细胞分为空白对照(Con)组、H/R组、对照质粒转染(miR-NC)组、miR-150-5p转染(miR-150-5p)组和miR-150-5p/茴香霉素(Anisomycin)[c-Jun氨基末端激酶(JNK)激活剂]组。通过实时荧光定量聚合酶链反应(RT-qPCR)检测各组细胞miR-150-5p表达；CCK-8法评估细胞增殖能力；通过流式细胞术检测细胞凋亡率；Western印迹分析JNK信号通路相关蛋白及凋亡相关蛋白表达。体内实验中，采用C57BL/6小鼠建立MIRI模型，分为对照(Sham)组、MIRI组和miR-150-5p过表达(miR-150-5p)组。原位注射腺病毒载体上调miR-150-5p表达。再灌注24 h后，麦胚凝集素(WGA)染色评估心肌纤维间隙及细胞外基质变化，并使用心脏超声评估心功能。酶联免疫吸附试验(ELISA)检测血清中心肌损伤标志物[肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)]及炎症因子[白细胞介素(IL)-6、肿瘤坏死因子(TNF)-α]水平。结果 体外实验中，与H/R组比较，miR-150-5p组和miR-150-5p/Anisomycin组凋亡率、p-JNK/JNK表达显著降低，miR-150-5p组Bax、Caspase-3蛋白表达显著降低，Bcl-2蛋白表达显著升高(P<0.05);与miR-NC组比较，miR-150-5p/Anisomycin组凋亡率、p-JNK/JNK表达显著降低(P<0.05),miR-150-5p组Bax、Caspase-3蛋白表达显著降低，Bcl-2蛋白表达显著升高；与miR-150-5p组比较，miR-150-5p/Anisomycin组凋亡率、p-JNK/JNK表达显著升高(P<0.05)。体内实验中，与MIRI组比较，miR-150-5p组miR-150-5p mRNA表达显著升高，LDH、CK-MB、TNF-α、IL-6水平、心肌细胞面积及凋亡率显著降低(P<0.05)。结论 miR-150-5p通过调控JNK信号通路，减少H/R诱导的心肌细胞凋亡，并在MIRI中减轻心肌细胞损伤，发挥保护作用。
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基本信息:
中图分类号:R542.2
引用信息:
[1]康树坝,何向辉,吕洪福,等.miR-150-5p在小鼠心肌缺血再灌注损伤中的作用机制[J].中国老年学杂志,2026,46(10):1896-1900.
2026-05-22
2026-05-22