目的 探讨低温复合黄芩素苷脑保护作用的机制.方法 采用四血管阻断法制作SD大鼠脑缺血-再灌注损伤模型.动物随机分成五组:假手术组(Sham组)、模型对照组(C组)、黄芩素苷组(B组)、低温组(HT组)、低温复合黄芩素苷组(HB组),后四组再分为再灌注2d和4 d两个亚组,每组5只.缺血期所有动物的脑温均控制在(37.0±0.5)C,再灌注6h期间HT组和HB组维持脑温在(32.0±0.5)℃,其余组则维持于(37.0±0.5)C.再灌注2d和4d时处死动物,分离海马CA1区,采用Western blot和RT-PCR法测定GluR2蛋白及其mRNA的表达.结果 再灌注2d和4d,C组GluR2蛋白及其mRNA灰度值较Sham组明显降低,B组、HT组明显高于C组,HB组高于B组及HT组(P＜0.01).结论 低温和黄芩素苷能抑制脑缺血后海马CA1区神经元GluR2蛋白及其mRNA的下调,两者合用的抑制作用更为明显.%Objective To investigate the mechanism of hypothermia combined-with breviscarpin for protecting the brain from ischemia-reperfusion injury in rats. Methods SD rats were randomly divided into five groups of Sham(sham-operated).C(model control), B( pretreated with breviscarpin). HT(hypothermia) and HB(hypothermia combined with breviscarpin). The rats of the last four groups were devided into two subgroups of reperfusion for 2 days and 4 days with 5 rats each. The brain temperature in groups of Sham. C and B was maintained at (37. 0 ± 0. 5) C until recovered from surgery. The brain temperature in groups of HT and HB was maintained at (32. 0 ± 0. 5) C for 6 hours during reperfusion. The rats were sacrificed and the hippocampal CA1 was removed in 2 or 4 days after reperfusion. GluR2 receptor expression was assessed by Western blot RT PCR was performed to assess the expression of GluR2 mRNA. The density of the bands was analyzed by the Software Image J for quantitation of GluR2 receptor/GluR2 mRNA expressioa Results The expressions of GluR2 receptor and GluR2 mRNA were lower in group C than those in group Sham in 2 and 4 days after cerebral ischemia CP<0. 01), which were higher in groups of B and HT than those in group C, and were higher in group HB than those in groups of B and HT at the corresponding time points (P<0. 01). Conclusion Both hypothermia and breviscarpin can attenuate the down-regulation of GluR2 receptor and GluR2 mRNA after brain ischemia, for which the effect of hypothermia combined with breviscarpin is better than that of hypothermia or breviscarpin alone.
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