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为研究IL 1β、TNF α及NO在感染性脑水肿时的变化和热休克反应对它们的影响 ,探讨热休克反应对大鼠感染性脑水肿的保护作用是否与其有关。本实验采用ELISA法和Griess法分别检测各组大鼠脑组织匀浆中IL 1β、TNF α及NO的含量。大鼠分为 3组 :①正常对照组 (NS ) ;②感染性脑水肿组 (PB ) ;③热休克处理组 (HS +PB )。每组又分为 4h、 8h、 2 4h三个时间点。结果显示 :与NS组比较 ,4h、 8h、 2 4hPB组的TNF α和NO含量明显增加 ,以 8h为最明显 (P <0 0 1或P <0 0 5 ) ;而在 4h、 8hPB组中 ,脑组织IL 1β含量明显增高 ,以 8h增高最明显 (P <0 0 1或P <0 0 5 ) ,2 4hPB组IL 1β含量明显下降。热休克反应能降低IL 1β、TNF α和NO在脑组织中的含量 ,在统计学上均有显著性意义 (P <0 0 1或P <0 0 5 )。以上结果表明IL 1β、TNF α及NO参与了感染性脑水肿的病理过程 ,热休克反应能减轻感染性脑水肿可能与其抑制IL 1β ,TNF α及NO生成有关
To investigate the changes of IL-1β, TNFα and NO in infectious brain edema and the effect of heat shock on them, and to explore whether the protective effects of heat shock response on infectious brain edema are related to them. In this study, ELISA and Griess method were used to detect the levels of IL-1β, TNF-α and NO in the homogenate of rat brain tissue. Rats were divided into three groups: ① normal control group (NS); ② infectious brain edema group (PB); ③ heat shock treatment group (HS + PB). Each group is divided into 4h, 8h, 24h three time points. The results showed that compared with the NS group, the levels of TNFα and NO in 4h, 8h, 24h PB group were significantly increased (P <0.01 or P <0 05), while in 4h, 8h PB group , The level of IL 1βin brain tissue increased significantly, which was the highest at 8h (P <0.01 or P <0.05). The level of IL 1β in 24 hPB group was significantly decreased. Heat shock response decreased the levels of IL-1β, TNF-α and NO in the brain, which were statistically significant (P <0.01 or P <0.05). The above results indicate that IL 1β, TNFα and NO are involved in the pathological process of infectious brain edema. Heat shock response may reduce the incidence of infectious brain edema possibly related to the inhibition of IL 1β, TNFα and NO production