宋朝彦 谢东 董晓辉 董轩 王春生.大鼠脑创伤后caspase-3的过度表达与细胞凋亡的关系[J].现代生物医学进展英文版,2014,14(24):4666-4669. |
大鼠脑创伤后caspase-3的过度表达与细胞凋亡的关系 |
The Excessive Expression of Caspase-3 and the Apoptosisafter Traumatic Brain Injury in Rats |
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DOI: |
中文关键词: 大鼠 颅脑创伤 casepase-3 凋亡 |
英文关键词: Rats Traumatic brain injury Caspase-3 Apoptosis |
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中文摘要: |
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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