HOTAIR靶向miR-138介导TLR4依赖性信号通路对脓毒症大鼠炎症和氧化应激作用机制
Chinese Journal of Public Health（2021）
Abstract
目的 探讨长链非编码RNA HOTAIR靶向miR-138并介导TLR4依赖性信号通路对脂多糖(LPS)诱导的脓毒症大鼠炎症反应和氧化应激的影响及其作用机制.方法 将大鼠按体重随机分为4组:对照组、模型组、shRNA对照组和shHOTAIR组,每组10只;腹腔注射脂多糖(5 mg/kg)建立脓毒症大鼠模型,采用RT-PCR法检测lncRNA HOX反义转录RNA(HOTAIR)和miR-138表达情况;苏木素-伊红染色观察各组大鼠肝、肺组织的病理损伤情况,试剂盒法检测肿瘤坏死因子a(TNF-a)、白细胞介素-6(IL-6)、IL-4和IL-10及超氧化物歧化酶(SOD)、丙二醛(MDA)和谷胱甘肽(GSH)表达水平,TLR4、NF-κB P65的磷酸化情况.结果 与对照组比较,模型组大鼠肺组织中HOTAIR表达升高、miR-138表达下降(P＜ 0.05).与对照组比较,模型组大鼠肝、肺组织出现明显的病理改变;与模型组比较,shHOTAIR组大鼠肝、肺组织病理改变明显减轻.与对照组比较,模型组大鼠血清中TNF-a、IL-6、MDA含量明显升高,IL-4、IL-10、SOD和GSH含量明显下降(P＜0.05);与模型组比较,shHOTAIR组大鼠血清中TNF-a、IL-6、MDA含量明显下降,IL-4、IL-10、SOD和GSH含量明显升高(P＜0.05).结论 HOTAIR通过靶向miR-138并介导TLR4依赖性的信号通路,抑制脂多糖诱导的脓毒症大鼠炎症反应和氧化应激.
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