miR-223抑制肺结核大鼠肺部病变

miR-223 inhibits pulmonary lesions of rats with pulmonary tuberculosis

目的探究miR-223对大鼠肺结核(PT)肺部病变、IFN-γ蛋白表达的作用机制。方法将大鼠分为正常组(NC组)、肺结核大鼠模型组(PT组)和肺结核大鼠模型注射miR-223 mimics组(miR-223组),每组10只。流式细胞仪检测外周血T细胞群,ELISA检测血清中IFN-γ和IL-18水平,并检测结核杆菌菌落数;HE染色观察肺组织病变;免疫组化检测肺组织中IFN-γ蛋白;RT-qPCR检测肺组织中miR-223 mRNA和IFN-γmRNA表达。结果PT组外周血T细胞亚群紊乱,CD3%、CD4%水平降低,CD8%水平升高(P<0.05);miR-223组CD3%、CD4%水平较PT组增加,而CD8%水平降低(P<0.05)。PT组血清中IFN-γ和IL-18水平较NC组增加(P<0.05);miR-223组较PT组得到明显抑制(P<0.05)。PT组结核杆菌菌落数较NC组增多(P<0.05);miR-223组结核杆菌菌落数较PT组明显减少(P<0.05)。PT组肺组织总IFN-γ表达较NC组明显升高(P<0.05);miR-223组较PT组得到明显抑制(P<0.05)。结论miR-223可抑制结核分枝杆菌引起的大鼠肺部炎性反应,并且miR-223也有抗结核杆菌和调节机体免疫的作用,同时还能有效抑制肺组织中IFN-γ的表达,进而降低结核病的严重程度。

Objective To explore the effect of miR-223 on pulmonary lesions and IFN-γ in rats with pulmonary tuberculosis(PT) mechanism of protein expression. Methods Rats were divided into normal group(NC group), pulmonary tuberculosis rat model group(PT group) and pulmonary tuberculosis rat model transfected with miR-223 mimics group(miR-223 group) with 10 in each group. T cells in peripheral blood was quantified by flow cytometry, IFN-γ in serum was detected by ELISA and IL-18 levels, and the number of Mycobacterium tuberculosis colonies was counted;the pathological changes of lung tissue were micros copied by HE staining;IFN-γ in lung tissue was detected by immunohistochemistry method;RT-qPCR was used to detect miR-223 mRNA and IFN-γ in lung tissue MRNA expression. Results In PT group, the peripheral blood T cell subsets were disordered, the level of CD3,CD4% significantly decreased, and CD8% was increased(P<0.05);CD3and CD4percentage inmiR-223 group were higher than those in PT group, while the percentage of CD8was lower(P<0.05). Serum IFN-γ and IL-18 in PT group increased(P<0.05);the number of Mycobacterium tuberculosis colonies in PT group was more than that in NC group(P<0.05);the colony number of Mycobacterium tuberculosis in miR-223 group was significantly less than that in PT group(P<0.05). Total IFN-γ level in PT group was higher than that in NC group(P<0.05) but was significantly inhibited in miR-223 group(P<0.05). Conclusions miR-223 can inhibit the pulmonary inflammatory response caused by Mycobacterium tuberculosis, and miR-223 showed an effect of anti-tuberculosis bacteria and may regulate host immunity, so and can effectively inhibit the expression of IFN-γ in lung tissue and thus alleviates severity of tuberculosis.