大鼠脑创伤后caspase-3的过度表达与细胞凋亡的关系

目的：探讨大鼠脑创伤后海马神经组织中casepase-3表达及其在细胞凋亡中的机制。方法：雄性Wistar大鼠72只随机分成对照组和创伤组。用Marmarou方法造成大鼠重型弥漫性颅脑创伤，采用免疫组织化学检测海马CA1区神经细胞casepase-3蛋白表达情况，原位细胞DNA断裂检测末端标记（TUNEL）法观察大鼠海马CA1区神经细胞凋亡动态变化。同时行TUNEL与caspase-3双标染色。结果：对照组海马区神经细胞casepase-3未见明显表达，创伤组海马CA1区神经细胞casepase-3表达在伤后3小时开始升高，伤后3天达高峰（P〈0．01），伤后7天下降明显。对照组海马区未见TUNEL阳性细胞，创伤组海马区TUNEL阳性细胞伤后3小时开始增多，伤后3天达高峰（P〈0．01），伤后7天下降。可见创伤组TUNEL染色与caspase-3免疫染色双标阳性的细胞伤后6小时细胞数量逐渐增多，于伤后3天达高峰（P〈0．01），伤后7天双标阳性细胞数量下降。Casepase-3表达与TUNEL阳性细胞明显相关（P〈0．01）。结论：大鼠脑创伤后casepase-3的过度表达是影响大鼠脑创伤后神经细胞凋亡原因之一，抑制casepase-3活性表达对神经组织起保护作用。

The Excessive Expression of Caspase-3 and the Apoptosis after Traumatic Brain Injury in Rats

Objective： To explore casepase-3 expression and the role of casepase-3 in apoptosis following traumatic brain injury （TBI） in rats. Methods： 85 male Wistar rats were randomly divided into 2 groups. According to Marmarou, severe closed brain injury was made. After that, immunohistochemical staining with caspase-3 were performed. TUNEL in situ was applied. At last, double staining with caspase-3 and TUNEL were performed. Results： Caspase-3 immunoreactivity in trauma group began to increase at 3h following injury, peaked at 3d （P〈0.01） and began to decline at 7d. At 3h in trauma group, a little TUNEL positive cell appeared in hippocampus, peaked at 3d （P〈0.01） and began to decline at 7d. The double positive cell in trauma group began to increase at 6h following injury, peaked at 3d （P〈0.01） and began to decline at 7d. The expression of casepase-3 was correlated with TUNEL positive cells （P〈0.01）. Conclusions： Excessive expressed and activated caspase-3 related to apoptosis, which plays an important part in the mechanism of nerve cell death. Certain neroprotective effect may be obtained by inhibiting excessive expression of caspase-3 caused by TBI.