摘要
目的探讨细胞凋亡在反复高 +Gz暴露所致脑损伤中的病理作用。方法 2 0只SD大鼠随机分成对照组、+Gz重复暴露后 30min、6h、2 4h和 48h 5组 ,每组 4只。对照组大鼠G值为 + 1Gz,实验组大鼠在动物离心机上经历了 3次 + 1 4Gz/45s(两次间间隔 30min)作用。分别于暴露后 30min、6h、2 4h和 48h处死大鼠取脑 ,固定包埋。用原位末端标记法 (TUNEL)检测大鼠海马细胞凋亡及用免疫组化方法检测凋亡相关基因bcl 2和 p53表达的变化。结果对照组和 +Gz重复暴露后 30min组海马各亚区未见凋亡细胞和bcl 2、p53表达变化 ,6h组海马CA1区可见部分细胞凋亡和明显的bcl 2、p53表达变化 ,但在 2 4h组和 48h组基本恢复正常。结论 +Gz重复暴露可引起大鼠海马细胞凋亡及凋亡相关基因bcl 2和 p53的表达变化 ,细胞凋亡是反复高Gz暴露致脑损伤的机制之一。
Objective To investigate the role of apoptosis in mechanisms of brain damage induced by repeated +Gz exposures. Method Twenty concious SD rats were randomly divided into 5 groups. Rats in the control group (n=4) were exposed to +1 Gz and rats in the 4 experimental groups (n=16) were exposed to +14 Gz for three times, each for 45 seconds with 30 min interval in between. All the +Gz exposured were on an animal centrifuge. The rat brains were taken 30 min, 6 h, 24 h and 48 h after the last centrifuge run and fixed and embeded. The apoptosis and expression changes of related gene bcl 2 and p53 were detected by terminal deoxynuleotide transferase mediated dUTP nick end labeling (TUNEL) technique and immunohistochemical method, respectively. Result Apoptotic cells and expression changes of bcl 2 and p53 were observed in CA1 subregion of rat hippocampus taken 6 h after repeated +Gz exposures, but returned to normal after 24～48 h. Conclusion It suggests that apoptosis and expression changes of bcl 2 and p53 in rats hippocampus can be induced by repeated +Gz exposures and the apoptosis is one of the molecular mechanisms of brain damage induced by repeated +Gz exposures.
出处
《航天医学与医学工程》
CAS
CSCD
2000年第4期263-266,共4页
Space Medicine & Medical Engineering
基金
全军医药卫生科研基金!课题 ( 98D0 3 3 )
空军后勤部科研基金
