【摘要】 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4d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)℃,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)℃。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。更多还原

【Abstract】 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)℃ until recovered from surgery. The brain temperature in groups of HT and HB was maintained at(32.0±0.5)℃ 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 expression. ResultsThe 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(P<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.更多还原