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目的探索维生素D对结核杆菌Mr19 000脂蛋白诱导的人类巨噬细胞损伤的作用。方法首先从健康志愿者血样中提取人巨噬细胞,同时从结核杆菌中制备Mr19 000脂蛋白。MTT法检测了Mr19 000脂蛋白以及1,25(OH)2D3对巨噬细胞增殖的作用,流式细胞术则用来评价二者对巨噬细胞凋亡的影响。接下来,我们通过MTT、FCM和ELISA等方法深入探究了维生素D对Mr19 000脂蛋白诱导的巨噬细胞损伤的作用及其机制。结果 16μg/ml Mr19 000脂蛋白作用巨噬细胞24 h后可显著减低巨噬细胞增殖并诱导巨噬细胞凋亡。相反,维生素D对人类正常巨噬细胞几乎没有毒性作用,能够阻断Mr19 000脂蛋白对巨噬细胞的损害。除此之外,维生素D还明显降低了Mr19 000脂蛋白诱导的NO/i NOS水平。结论维生素D可通过调控NO/i NOS水平阻碍结核杆菌毒力因子Mr19 000脂蛋白诱导的人类巨噬细胞凋亡。
Objective To explore the effect of vitamin D on the injury of human macrophages induced by M. tuberculosis Mr19 000 lipoprotein. Methods Firstly, human macrophages were extracted from blood samples of healthy volunteers and Mr19 000 lipoprotein was prepared from Mycobacterium tuberculosis. The effects of Mr19000 lipoprotein and 1,25 (OH) 2D3 on the proliferation of macrophages were detected by MTT assay. Flow cytometry was used to evaluate the effects of both Mr19000 lipoprotein and macrophage apoptosis. Next, we investigated the effect and mechanism of vitamin D on Mr19 000 lipopolysaccharide-induced macrophage injury by MTT, FCM and ELISA. Results Macrophages treated with Mr19 000 lipopolysaccharide at a dose of 16μg / ml for 24 h significantly reduced macrophage proliferation and induced macrophage apoptosis. In contrast, vitamin D has almost no toxic effect on human normal macrophages and blocks the destruction of macrophages by Mr19 000 lipoprotein. In addition, vitamin D also significantly reduced Mr19 000 lipoprotein-induced NO / i NOS levels. Conclusion Vitamin D can block the apoptosis of human macrophages induced by Mycobacterium tuberculosis virulence factor Mr19 000 by regulating NO / i NOS level.