甲基强的松龙对大鼠颅脑损伤后细胞间黏附分子-1的影响

Effects of methylprednisolone on brain tissue ICAM-1 after brain trauma of rats

目的 观察甲基强的松龙对大鼠颅脑损伤后脑组织中细胞间黏附分子 (ICAM ) 1含量的影响 ,探讨其作用机制。方法 将 5 5只SD大鼠随机分为 3组 ,采用骨窗形成后硬膜外打击法造成鼠脑挫裂伤模型 ,正常组 5只 ,麻醉后 ,只行开颅手术 ,不作头颅打击 ;治疗组致伤后腹腔内注射 3 0mg/kg体重甲基强的松龙 ,对照组腹腔内注射 3 0mg/kg体重生理盐水。对照组和治疗组分别在伤后 6、2 4、48、72、96h断头取脑 ,对脑组织中ICAM 1含量进行检测。结果 治疗组脑皮质中的ICAM 1活性在伤后 6h较对照组升高 (P <0 .0 1) ,48h达高峰后开始下降 ,96h降至基础水平。甲基强的松龙治疗组在伤后 6～ 48hICAM 1活性较对照组明显降低 (P <0 .0 5 )。结论 颅脑损伤后 ,受损脑组织中ICAM 1含量升高 ,甲基强的松龙可通过抑制损伤后ICAM 1活性 ,起到保护创伤神经元的作用。

Objective To observe the effects of methylprednisolone on the change of ICAM-1 level in brain trauma tissue of rat.Methods Fifty-five rat brain traumatic models were made by frontoparictal bone window plasty with extradural hitting.The rats were divided to three groups: treated group (treated with methylprednisolone,30 mg/kg after hitting),contral group (treated with physiologic saline after hitting) and normal group (only expose extradural without hitting and injection).The levels of ICAM-1 were measured at different time points after hitting.Results ICAM-1 level in rat cerebral cortes was higher in treated group than that in the contrl group post-traumatic 6 h,reached the peak post-traumatic 48 h and dropped to the basic level post-traumatic 72 h.The levels of ICAM-1 in treated group was obviously lower than in control group post-traumatic 6-48 h.Conclusion Methylprednisolone could pretect the traumatic neurons by inhibiting the activity of ICAM-1 which was increased in the injured brain tissues after brain injury.