亚低温减轻沙土鼠脑缺血／再灌注损伤与海马CAl区Bax表达变化的关系

目的研究亚低温（33℃，4h）减轻沙土鼠脑缺血／再灌注损伤与海马CA1区Bax表达变化的关系，探讨亚低温脑保护的可能机制。方法采用沙土鼠双侧颈总动脉阻断5min前脑缺血／再灌注损伤模型，随机分为假手术组（SH）、常温再灌注组（IR）、低温假手术组（HSH）、低温再灌注组（HIR），每组根据再灌注的不同时间点（2h、4h、1d、3d、5d）又分为5个对应的亚组（／Z=6）。在预定时间点行开阔法迷宫检查，TUNEL法检测海马CA1区的凋亡细胞，苏木精-伊红染色检测海马存活细胞，免疫组化检测Bax在海马CA1区的动态变化。结果4h亚低温可显著减少缺血沙土鼠1d、3d、5d的探索活动及CA1区的凋亡细胞，增加存活细胞，抑制脑缺血后海马CA1区Bax的早期表达（2h、4h、1d）。结论4h亚低温对沙土鼠5min前脑缺血有确切的保护作用，抑制海马CA1区缺血／再灌注早期Bax的表达可能是其减少海马细胞凋亡、产生脑保护作用的机制之一。

The relationship between mild hypothermia alleviating cerebral ischemic/reperfusion injury and the level of Bax in hippocampal CA1 regions after cerebral ischemi.c/reperfusion in gerbils

Objective To explore the relationship between the effects of mild hypothermia on cerebral ischemic/ reperfusion injury and expressions of Bax in hippocampal CAI area after forebrain ischemia at the different spots in gerbils and to discuss the possible mechanism of mild hypothemia for brain protection. Methods Forebrain ischemic model in- duced by bilateral common carotid artery obstruction was adopted. The gerbils were randomly divided into 4 groups ： sham group（SH） ： sham operated group having the same surgical procedures without bilateral carotid arteries occlusion; normo-thermic ischemic reperfusion （IR） group： having a 5 min ischemia; hypothernaia sham （HSH） group： having the same operation as SH and cooling body temperatures at 33 ℃ ± 0.5 ℃ for 4 h ; hypothermic ischemic reperfusion （HIR） group ： having a 5 min ischemia and immediately after reperfusion cooling body temperatures at 33℃ ± 0.5℃ for 4 h. At differ-ent time spots after ischemia, with the animals designated as subgroups 2 h, 4 h, 1 d, 3 d, 5 d（n =6 in each）. The ani-mals＇ behavior was observed by open field method. The apoptotic neurons were detected in CA1 area by TUNEL method. The survival neurons of hippocampal CA1 regions were accounted on H - E staining slides. The expression of Bax in hip- pocampal CA1 area was detected by SP immunocytochemical technique. Results The behavioral marks and the number of apoptotic neuons in hippocampal CA1 region were much less in HIR group than in IR group. The number of survival neurons in hippocampal CA1 region in HIR group was more than that in IR group. The expression of Bax was reduced in the CA1 area in HIR group than in IR group at early reperfusion（2 h, 4 h, ld）. Conclusions Hypothermia can signifi-cantly protect neurons against cerebral ischemia, and its protective mechanism involves reducing Bax activation at early reperfusion.