苦碟子总黄酮对大鼠脑缺血再灌注损伤的保护作用

目的研究苦碟子总黄酮(TFS)对大鼠全脑缺血再灌注损伤的保护作用。方法按pulsinelli方法制成全脑缺血模型,大鼠全脑缺血30min后再灌注40min。记录脑缺血前、缺血30min及再灌注40min后的脑电图(EEG),取脑组织,采用荧光指示剂Fura-2定量测定大鼠前脑皮层组织细胞内游离钙离子浓度,测定超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、乳酸脱氢酶(LDH)、一氧化氮合酶(NOS)活性和丙二醛(MDA)、一氧化氮(NO)含量。结果 TFS可促进缺血后EEG的恢复,降低缺血再灌后细胞内游离钙离子浓度的升高,抑制SOD、GSH-Px和LDH活力的下降,降低NOS的活力和脑组织中MDA、NO的含量。结论 TFS对脑缺血再灌注损伤有显著的保护作用,其机制可能与其抗自由基、抑制钙超载和NO生成有关。

Protective Effects of Total of Flavonoids of Sowthistle-leafixeris Seedling on Cerebral Ischemia-reperfusion Injury in Rats

Objective To investigate the protective effects of Total of flavonoids of sowthistle-leafixeris seedling（TFS） against cerebral ischemia-reperfusion injury.Methods Four-vessel occlusion method was used to make acute cerebral ischemia-reperfusion model.The brain of rats was initiated by ischemia for 30min followed by 40min of reperfusion.The electroencephalography（EEG） during cerebral ischemia and reperfusion was recorded.The level of intracellular calcium ion concentration（Ca2＋]i） in cerebral cells after ischemia was treated by using a Ca2＋ indicator Fura-2/AM.Superoxide dismutase（SOD）,glutathione peroxidase（GSH-Px）,Lactate dehydrogenase（LDH）,nitric oxide synthase（NOS） activeties and malondialdehyde（MDA）,nitric oxide（NO） contents in the ischemia cerebral cortex were measured.Results TFS can improved the EEG change,significantly reduced the decreases of the intracellular calcium ion concentration（Ca2＋]i）,remarkly increased GSH-Px,SOD and NOS activities in the cerebrum.Inhibit the decrease of LDH activity and NO,MDA contents.Conclusion TFS has profective effects on cerebral ischemia-reperfusion injury,the mechanism may relate to attenuating free radical,Ca2＋]i overload and NO.