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大鼠脑外伤后神经细胞凋亡与Bcl-2蛋白的关系
引用本文:陈江利,刘伟国,方乃成,何玉领,杨刚. 大鼠脑外伤后神经细胞凋亡与Bcl-2蛋白的关系[J]. 浙江创伤外科, 2006, 11(5): 377-379
作者姓名:陈江利  刘伟国  方乃成  何玉领  杨刚
作者单位:1. 310009,杭州,浙江大学医学院附属第二医院
2. 浙江省诸暨市人民医院
摘    要:目的研究大鼠外伤性脑挫裂伤细胞周围水肿带细胞凋亡随出血时相点的变化规律,以及脑挫裂伤后神经细胞凋亡和Bcl-2的关系.为脑挫伤的治疗提供理论依据。方法将健康Wistar大鼠随机分成6组,10只为对照组,50只为实验组,设置为6小时、24小时、3天、5天、7天共5个时相点.术后制作冰冻切片。用末端脱氧核糖转移酶介导的生物素化脱氧尿嘧啶缺刻标记技术(TUNEL技术)和免疫组化法(SP法1观察凋亡细胞和Bcl-2蛋白的表达..结果在正常脑组织中bcl-2表达为阴性。损伤早期细胞凋亡与bcl-2表达明显增加,随着伤后时间延长.凋亡细胞伤后第3天达到高峰.而Bcl-2表达5天达到峰值。结论细胞凋亡与Bcl-2蛋白表达在一定时间窗内持续升高,但不同步,两者无明显线性关系.表明了bcl-2基因的抑制细胞凋亡作用。

关 键 词:脑挫裂伤  bcl-2基因  细胞凋亡
收稿时间:2006-03-20
修稿时间:2006-03-20

Relationship between apoptosis and expression of Bcl-2 after cerebral trauma in rats
CHEN Jiangli, LIU weiguo, FANG naicheng,et al.. Relationship between apoptosis and expression of Bcl-2 after cerebral trauma in rats[J]. Zhejiang Journal of Traumatic Surgery, 2006, 11(5): 377-379
Authors:CHEN Jiangli   LIU weiguo   FANG naicheng  et al.
Affiliation:The second Affiliated Hospital,zhejiang University, Medical college.Hangzhou, Zhejiang, 310009, China
Abstract:Objective To explore the change of apoptosis around the hematoma after cerebral injury and relationship between apoptosis and expression of bcl-2. Methods Sixty healthy male Wistar rats were divided into six groups as follows:6hours, 24hours, 3days, 5days, 7days after being sacrificed on schedule.The number of the apoptosis cell and bcl-2 gene expression analysis were observed by terminal deoxynucleotidy transferase mediated dUTPbiotin nickend labeling(TUNEL). Results In normal groups, bcl-2 gene expression could not be detected.The expression of bcl-2 increased as the apoptosis in early period with its peak at 5 days. While the number of apotosis cells decreased with its peak at 3 days. Conclusion The expression of Bcl-2 protein and cell apoptosis keeps increasing during certain period after cerebral injury without obvious linear relationship between apoptosis and expression of Bcl-2 protein.Its indicated that Bcl-2 has the effect on inhibiting apoptosis.
Keywords:cerebral injury   bcl-2 gene   apoptosis.
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