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机构地区:[1]南通大学附属医院小儿外科 [2]南通大学人体解剖学教研室,江苏南通226001
出 处:《实用儿科临床杂志》2009年第23期1800-1801,1819,共3页Journal of Applied Clinical Pediatrics
基 金:江苏省高校自然科学研究指导性计划项目资助(05KJD180165)
摘 要:目的探讨额叶锐器损伤后幼鼠神经细胞凋亡的变化规律及调控机制。方法采用末端脱氧核苷酸转移酶介导的原位缺口末端标记法(TUNEL)进行细胞凋亡检测,观察伤后幼鼠细胞凋亡变化;采用免疫组织化学染色方法观察其创伤区及周边的Bax及Bcl-2阳性细胞的表达变化。结果脑损伤1h后幼鼠创伤区及周边皮质即发现凋亡细胞,随伤程的推移,TUNEL阳性凋亡细胞数量逐渐增多,24h达到高峰,之后凋亡细胞数量逐渐下降,120h偶见少许凋亡细胞。创伤后1h幼鼠Bax阳性细胞的表达开始增高,12h达到高峰,之后逐渐下降,脑损伤后120h仅有少量表达。在伤后1h幼鼠Bcl-2的上调明显,Bcl-2阳性凋亡细胞数目达到高峰,随后Bcl-2的表达下调逐渐下降。脑损伤后120h仍见少部分表达。空白对照组及假手术组幼鼠额叶皮质中偶见Bax和Bcl-2阳性细胞表达;伤后Bax/Bcl-2比值上调,24h达到高峰,随后逐渐下降。结论幼鼠额叶锐器伤后存在细胞凋亡,凋亡细胞数量的变化与损伤后时程有关,Bax/Bcl-2比值是决定幼鼠细胞凋亡的重要因素。Objective To investigate the alterations and molecular mechanism of neural cell apoptosis after frontal lobe sharp injury in infant rats.Methods Brain damage was induced by frontal lobe sharp injury.dUTP nick end labeling(TUNEL) method was used to detect cell apoptosis after brain injury,and immunohistochemistry was used to detect the expression of Bax,Bcl-2 proteins in and around the area of injury,respectively.Results The apoptosis cells were found as early as 1 hour and reached a peak at 24 hours post-injury,then gradually diminished until 120 hours when only few apoptosis cells presented.The expression of Bax and Bcl-2 proteins increased significantly 1 hour after frontal lobe injury.Bax protein reached its peak at 12 hours while Bcl-2 protein reached its peak at 1 hour post-injury.The ratio of Bax to Bcl-2 increased after lesion with peak at 24 hours,and then decreased thereafter.At 120 hours,very weak expression of Bax and Bcl-2 protein detected.There were few Bax and Bcl-2 positive cells in frontal lobe cortex in blank control and sham operation group.Conclusions Cell apoptosis exists after frontal lobe sharp injury in infant rats and the change of the number of apoptotic cells is correlated with time course of post-injury.The ratio of Bax to Bcl-2 may play a vital role in cell apoptosis.
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