临床神经外科杂志
臨床神經外科雜誌
림상신경외과잡지
JOURNAL OF CLINICAL NEUROSURGERY
2015年
2期
107-110
,共4页
大鼠%颅脑创伤%casepase-3%凋亡%丁苯酞
大鼠%顱腦創傷%casepase-3%凋亡%丁苯酞
대서%로뇌창상%casepase-3%조망%정분태
rats%traumatic brain injury%caspase-3%apoptosis%dl-3-n-butylphthalide
目的:探讨丁苯酞在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作用。方法雄性Wistar大鼠120只随机分成3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casepase-3蛋白表达情况,末端标记( TUNEL)法观察大鼠脑内神经细胞凋亡动态变化。结果对照组海马区神经细胞casepase-3未见明显表达,创伤组海马区神经细胞casepase-3表达在伤后3 h开始升高,伤后3 d达高峰,伤后7 d下降明显。药物组海马区神经细胞casepase-3表达在伤后3 h开始升高,伤后3 d达高峰,高峰值低于创伤组(P<0.01),伤后7 d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6 h开始升高,3 d达高峰,伤后7 d下降。药物组海马区TUNEL阳性细胞伤后6 h开始升高,3 d达高峰,高峰值低于创伤组(P<0.05),伤后7 d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,丁苯酞可以抑制casepase-3活性表达,减少神经细胞凋亡,对神经组织起保护作用。
目的:探討丁苯酞在大鼠腦創傷後海馬神經組織中casepase-3錶達及其在細胞凋亡中的作用。方法雄性Wistar大鼠120隻隨機分成3組,用Marmarou方法造成大鼠重型瀰漫性顱腦創傷,採用免疫組織化學檢測casepase-3蛋白錶達情況,末耑標記( TUNEL)法觀察大鼠腦內神經細胞凋亡動態變化。結果對照組海馬區神經細胞casepase-3未見明顯錶達,創傷組海馬區神經細胞casepase-3錶達在傷後3 h開始升高,傷後3 d達高峰,傷後7 d下降明顯。藥物組海馬區神經細胞casepase-3錶達在傷後3 h開始升高,傷後3 d達高峰,高峰值低于創傷組(P<0.01),傷後7 d下降明顯。對照組海馬區未見TUNEL暘性細胞,創傷組海馬區TUNEL暘性細胞傷後6 h開始升高,3 d達高峰,傷後7 d下降。藥物組海馬區TUNEL暘性細胞傷後6 h開始升高,3 d達高峰,高峰值低于創傷組(P<0.05),傷後7 d下降。 casepase-3錶達與TUNEL暘性細胞明顯相關(P<0.01)。結論大鼠腦創傷後casepase-3的過度錶達是影響大鼠腦創傷後神經細胞凋亡原因之一,丁苯酞可以抑製casepase-3活性錶達,減少神經細胞凋亡,對神經組織起保護作用。
목적:탐토정분태재대서뇌창상후해마신경조직중casepase-3표체급기재세포조망중적작용。방법웅성Wistar대서120지수궤분성3조,용Marmarou방법조성대서중형미만성로뇌창상,채용면역조직화학검측casepase-3단백표체정황,말단표기( TUNEL)법관찰대서뇌내신경세포조망동태변화。결과대조조해마구신경세포casepase-3미견명현표체,창상조해마구신경세포casepase-3표체재상후3 h개시승고,상후3 d체고봉,상후7 d하강명현。약물조해마구신경세포casepase-3표체재상후3 h개시승고,상후3 d체고봉,고봉치저우창상조(P<0.01),상후7 d하강명현。대조조해마구미견TUNEL양성세포,창상조해마구TUNEL양성세포상후6 h개시승고,3 d체고봉,상후7 d하강。약물조해마구TUNEL양성세포상후6 h개시승고,3 d체고봉,고봉치저우창상조(P<0.05),상후7 d하강。 casepase-3표체여TUNEL양성세포명현상관(P<0.01)。결론대서뇌창상후casepase-3적과도표체시영향대서뇌창상후신경세포조망원인지일,정분태가이억제casepase-3활성표체,감소신경세포조망,대신경조직기보호작용。
Objective To explore the casepase-3 expression and role of casepase-3 in apoptosis following traumatic brain injury(TBI) in rat and the effect of dl-3-n-butylphthalide(NBP).Methods 120 male Wistar rats were randomly divided into 3 groups .According to Marmarou , severe closed brain injury was made .After that , immunohistochemical staining with Caspase-3 were performed of hippocampus CA1 region.TUNEL in situ was applied of the apoptosis cell in hippocampus CA 1 region.Double staining was to show the relation of apoptosis and Caspase -3.Results Caspase-3 in the trauma group began to increase at 3 h following injury , peaked at 3rd d and began to decline at 7 d. Caspase-3 in NBP treatment group was the same in each time , but in the peak , Caspase-3 was decreased in NBP treatment group compared with that in trauma group (P<0.01).At 3 h in trauma group , a little TUNEL positive cell appeared in hippocampus , peaked at 3rd d and began to decline at 7 d.TUNEL positive cell in NBP treatment group was the same in each time ,but in the peak , TUNEL positive cell was decreased in NBP treatment group compared with that in trauma group (P<0.05). The expression of casepase-3 was correlated with TUNEL positive cells ( P<0.01) .Conclusion NBP treatment in rats after TBI has certain neuroprotective effect , whose resistance roles in nerve cell apoptosis may be implemented by inhibiting excessive expressed caspase -3 caused by TBI .