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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 pathological role of apoptosis in brain injury induced by repeated high + Gz exposure. Methods Twenty SD rats were randomly divided into 4 groups: control group, + Gz repeated exposure 30min, 6h, 24h and 48h 5 groups. In the control group, the G value was + 1Gz, and the rats in the experimental group underwent three cycles of + 1 4Gz / 45s on an animal centrifuge (twice between intervals of 30 minutes). Rats were sacrificed 30min, 6h, 24h and 48h after exposure, respectively. The brains were fixed and embedded. The apoptosis of hippocampal cells was detected by TUNEL and the expressions of bcl-2 and p53 were detected by immunohistochemistry. Results No apoptotic cells and changes of bcl-2 and p53 were observed in the hippocampus in the control group and 30 minutes after + Gz exposure. Some apoptosis and significant changes of bcl-2 and p53 were observed in hippocampal CA1 area of 6h group 2 4h group and 48h group returned to normal. Conclusion Repeated + Gz exposure can induce the apoptosis of hippocampal cells and the expression of bcl-2 and p53 in hippocampus of rats. Apoptosis is one of the mechanisms of repeated Gz exposure-induced brain injury.