基于JAK2/STAT3信号通路探究调控miRNA-27a对肺结核大鼠的干预效果  

To explore the intervention effect of regulating miRNA-27a on pulmonary tuberculosis rats based on JAK2/STAT3 signaling pathway

作　　者：吴海燕[1] 林娟娟 戢晴 杨朝晖[1] 徐红艳 WU Haiyan;LIN Juanjuan;JI Qing;YANG Chaohui;XU Hongyan(Department of Infection,Taizhou First people's Hospital,Taizhou 318020,Zhejiang,China;Department of Emergency,Taizhou Hospital of Zhejiang Province,Taizhou 317000,Zhejiang,China;Department of Nephrology,Taizhou First People’s Hospital,Taizhou 318020,Zhejiang,China)

机构地区：[1]台州市第一人民医院感染科,浙江台州318020 [2]浙江省台州医院急诊科,浙江台州317000 [3]台州市第一人民医院肾内科,浙江台州318020

出　　处：《中国现代医生》2023年第14期6-10,共5页China Modern Doctor

基　　金：浙江省医药卫生科技计划项目(2023KY398)。

摘　　要：目的分析基于蛋白酪氨酸激酶2(janus kinase 2,JAK2)/信号转导因子和转录激活因子3(signal transducer and activator of transcription 3,STAT3)信号通路探究调控微RNA(microRNA,miRNA)-27a对肺结核大鼠的干预效果。方法选取50只雄性SPF级Wistar大鼠,采用随机数字表法选取10只大鼠作为对照组,另外40只建立肺结核模型,将建模成功的30只大鼠分为模型组(n=10)、沉默组(n=10)、过表达组(n=10)。对照组和模型组大鼠注射生理盐水,沉默组大鼠尾静脉注射10μl miRNA-27a沉默慢病毒悬液,过表达组大鼠尾静脉注射10μl miRNA-27a过表达慢病毒悬液。比较miRNA-27a表达量、结核分枝杆菌菌落数、γ干扰素(interferon-γ,IFN-γ)、白细胞介素6(interleukin-6,IL-6)、环氧化酶-2(cyclooxygenase-2,COX-2)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)表达水平,以及JAK2、STAT3 mRNA、JAK2、p-JAK2、STAT3、p-STAT3表达量水平。结果与对照组相比,模型组miRNA-27a表达量降低,结核分枝杆菌菌落数、IFN-γ、IL-6、COX-2、TNF-α、JAK2、STAT3 mRNA、JAK2、p-JAK2、STAT3、p-STAT3表达量升高,差异均有统计学意义(P<0.05);与沉默组相比,过表达组miRNA-27a表达量升高,结核分枝杆菌菌落数、IFN-γ、IL-6、COX-2、TNF-α、JAK2、STAT3 mRNA、JAK2、p-JAK2、STAT3、p-STAT3表达量降低,差异均有统计学意义(P<0.05)。结论上调miRNA-27a表达,可改善肺结核大鼠体内菌落水平,使大鼠肺损伤减轻,其机制可能抑制JAK2/STAT3信号通路相关。Objective To analyze the effect of the signal transducer and activator of transcription 3(STAT3)signalling pathway based on janus kinase 2(JAK2)on the regulation of microRNA(miRNA)-27a in rats with pulmonary tuberculosis.Methods A total of 50 male SPF-grade Wistar rats were selected.10 rats were selected as the control group according to the random number table method,and the other 40 were used to establish a tuberculosis model.Totally 30 rats were successfully modelled and divided into model group(n=10),silent group(n=10)and overexpression group(n=10).The rats in the control and model groups were injected with saline,the rats in the silent group were injected with 10μl of miRNA-27a silencing lentiviral suspension in the tail vein,and the rats in the overexpression group were injected with 10μl of miRNA-27a overexpression lentiviral suspension in the tail vein.Compared miRNA-27a expression,mycobacterium tuberculosis colony count,interferon-γ(IFN-γ),interleukin-6(IL-6),cyclooxygenase-2(COX-2),tumor necrosis factor-α(TNF-α)expression levels,as well as JAK2,STAT3 mRNA,JAK2,p-JAK2,STAT3,p-STAT3 expression levels.Results Compared with the control group,the model group showed decreased miRNA-27a expression and increased expression of mycobacterium tuberculosis colony number,IFN-γ,IL-6,COX-2,TNF-α,JAK2,STAT3 mRNA,JAK2,p-JAK2,STAT3,p-STAT3,all with statistically significant differences(P<0.05).Compared with the silent group,the overexpression group showed increased expression of miRNA-27a,IFN-γ,IL-6,COX-2,TNF-α,JAK2,p-JAK2,STAT3,p-STAT3.The expression of miRNA-27a was increased and the expression of Mycobacterium tuberculosis colony number,IFN-γ,IL-6,COX-2,TNF-α,JAK2,STAT3 mRNA,JAK2,p-JAK2,STAT3,p-STAT3 was decreased in the overexpression group compared with the silencing group,and the differences were all statistically significant(P<0.05).Conclusion Upregulation of miRNA-27a expression can improve colonization levels and reduce lung injury in rats with pulmonary tuberculosis by a mechanism that may be relate

关 键 词：肺结核 蛋白酪氨酸激酶2/信号转导因子和转录激活因子3 微RNA-27a 干预效果 

分 类 号：R521[医药卫生—内科学]