论文部分内容阅读
目的探讨不同毒力结核分枝杆菌对感染宿主巨噬细胞应激的调控作用。方法以结核分枝杆菌国际标准强毒株H37Rv菌株(简称H37Rv菌株)和卡介苗菌株(简称BCG)分别感染小鼠巨噬细胞RAW264.7,在感染1、6、12、24h后,分别采用化学比色法检测感染巨噬细胞超氧化物歧化酶(SOD)和一氧化氮合酶(NOS)的活性变化,并测定感染巨噬细胞的丙二醛(MDA)和一氧化氮(NO)含量变化。结果 RAW264.7感染BCG后细胞内SOD、NOS活性和NO含量逐渐升高,感染24h分别为(32.82±0.54)U/ml、(12.16±0.29)U/ml和(116.42±3.23)μmol/L,与对照组比较差异有统计学意义(P<0.05);MDA含量逐渐下降,感染24h时为(0.59±0.08)nmol/ml,与对照组比较差异有统计学意义(P<0.05);RAW264.7感染H37Rv菌株后细胞内SOD、NOS和NO含量逐渐下降,感染24h分别为(15.90±0.20)U/ml、(2.32±0.11U/ml)和(13.74±1.01μmol/L),与对照组比较差异有统计学意义(P<0.05):MDA含量逐渐增加,感染24h时为(5.21±0.39)nmol/ml,与对照组比较差异有统计学意义(P<0.05)。结论低毒力和高毒力结核分枝杆菌分别对感染宿主巨噬细胞的应激发挥诱导和抑制等不同作用。
Objective To investigate the regulatory effect of different virulence of Mycobacterium tuberculosis on host macrophages in response to stress. Methods Mouse macrophage RAW264.7 cells were infected with the H37Rv strain of Mycobacterium tuberculosis (referred to as H37Rv strain) and BCG strain (BCG for short), respectively. After infection for 1, 6, 12 and 24 hours, The activity of superoxide dismutase (SOD) and nitric oxide synthase (NOS) in infected macrophages were detected by colorimetric assay. The levels of malondialdehyde (MDA) and nitric oxide (NO) Variety. Results The activities of SOD, NOS and NO in RAW264.7 cells after infection with BCG increased gradually (32.82 ± 0.54) U / ml, (12.16 ± 0.29) U / ml and (116.42 ± 3.23) μmol / L (P <0.05). The content of MDA decreased gradually (0.59 ± 0.08) nmol / ml at 24h, and the difference was statistically significant compared with the control group (P <0.05) .7 The intracellular levels of SOD, NOS and NO gradually decreased after infection with H37Rv strain and reached (15.90 ± 0.20) U / ml, (2.32 ± 0.11U / ml) and (13.74 ± 1.01μmol / L) The difference was statistically significant (P <0.05). The content of MDA gradually increased and reached (5.21 ± 0.39) nmol / ml at 24 hours of infection, which was significantly different from the control group (P <0.05). Conclusion Low-virulent and high-virulent Mycobacterium tuberculosis have different effects on the induction of host macrophages and their inhibition.