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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。

英文摘要:

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).Conclusion: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.

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