山茶花总黄酮对大鼠脑缺血再灌注损伤的保护作用

目的研究山茶花总黄酮(TFC)对大鼠全脑缺血再灌注损伤的保护作用。方法按pu lsinelli方法制成全脑缺血模型,大鼠全脑缺血30 m in后再灌注40 m in。记录脑缺血前、缺血30 m in及再灌注40 m in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TFC可促进缺血后EEG波幅的恢复,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TFC对脑缺血再灌注损伤有保护作用,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 flacone C on cerebral ischemia-reperfusion injury in rats

Aim To study protective effects of Total of flacone C(TFC) against cerebral ischemia-reperfusion injury.Methods Four-vessel occlusion method was used to make acute cerebral ischemia-reperfusion model. Rats were initiated by ischemia for 30 min followed by 40 min of reperfusion.The electroencephalography(EEG) during cerebral ischemia and reperfusion was recorded.The level of intracellular calcium ion concentration(Ca~(2+)]i) in cerebral cells after ischemia was measured by using a Ca~(2+) 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 TFC can improved the EEG change,significantly attenuated the decrease of the intracellular calcium ion concentration(Ca~(2+)]_i), remarkly increased GSH-Px,SOD and NOS activities in the cerebrum,inhibit the decrease of LDH activity and NO,MDA contents.Conclusion TFC has protective effects on cerebral ischemia-reperfusion injury,the mechanism may be related to attenuating free radical,Ca~(2+)]i overload and NO.