大鼠全脑缺血再灌流后脑组织P53及P21蛋白的表达

目的　探讨大鼠全脑缺血再灌流后Ｐ５３、Ｐ２１蛋白的表达及其与迟发性神经元死亡（ＤＮＤ）的关系。方法　在４ 血管闭塞法全脑缺血模型上，采用ＨＥ及ＬＳＡＢ染色法，观察脑组织病理改变，检测脑组织Ｐ５３、Ｐ２１蛋白的表达，以及蛋白合成抑制剂放线菌酮对其的影响。结果　全脑缺血１５ ｍ ｉｎ 再灌流后，脑组织Ｐ５３、Ｐ２１蛋白表达增加，且两者分布接近。海马结构、丘脑、下丘脑等白质区（再灌流后６ ｈ）较皮层、海马的神经细胞核（２４ ｈ）先检测到Ｐ５３、Ｐ２１蛋白，７２ ｈ 表达达高峰。并且以缺血损伤最严重的海马ＣＡ１ 区Ｐ５３、Ｐ２１蛋白表达为强。另外，放线菌酮可抑制脑组织Ｐ５３、Ｐ２１蛋白的表达，并对ＤＮＤ具有一定的保护作用。结论　全脑缺血再灌流损伤后，脑组织Ｐ５３、Ｐ２１蛋白表达增加，放线菌酮可抑制其表达，并对ＤＮＤ起保护作用，提示Ｐ５３、Ｐ２１蛋白参与了全脑缺血后ＤＮＤ的凋亡机制，并对其起促进作用

Expression of p53,p21 Proteins in Brain after Reperfusion Following Forebrain Ischemia

Objective To investigate the relationship between P 53 ,P 21 proteins and DND after reperfusion following forebrain ischemia in rats. Methods On four vessel occlusion model of ischemic brain tissue of rats, the pathologic expression of P 53 and P 21 proteins with the effects of protein synthesis inhibitor cycloheximide, using HE and LSAB staining techniques, was observed. Results The expression of P 53 and P 21 proteins was upregulated after reperfusion following 15 min forebrain ischemia. The distribution of P 53 and P 21 proteins were similar. The expression of P 53 and P 21 proteins in brain sections was detected earlier in the white matter of hippocampal formation, thalamus, and hypothalamus (6 h following reperfusion) than in the neuronal nuclei in cerebral cortex and CA1 region (24 h), and the maximal induction was observed at 72 h following reperfusion. CA1 region suffered the most serious injury with the positive expression of P 53 and P 21 proteins. On the other hand, cycloheximide could reduce the expression of P 53 and P 21 proteins in ischemic brain tissue also protect CA1 region from DND. Conclusions Reperfusion following forebrain ischemia lead to upregulation of the expression of P 53 and P 21 proteins in ischemic brain tissue, and cycloheximide could reduce their expression, also protect neurons from DND, suggesting P 53 and P 21 proteins participated the apoptosis process of DND.