摘要
目的:探讨黄芩苷抑制脑缺血-再灌注损伤的作用机制。方法:线栓法制作大脑中动脉缺血-再灌注大鼠模型。应用RT-PCR、Western-blot以及酶免疫测定方法,观察黄芩苷对环氧化物酶-2(COX-2)、5-脂加氧酶(5-LOX)及其代谢产物前列腺素E2(PGE2)和半胱氨酸白三烯(cys-LT)的影响。使用聚丙烯酰胺凝胶电泳检测脑组织清蛋白含量,评价黄芩苷对脑缺血-再灌时血脑屏障的影响。结果:①黄芩苷降低脑缺血-再灌注时组织细胞质内5-LOX的含量(P<0.01),抑制cys-LT的合成(P<0.01)。②黄芩苷减轻缺血-再灌注损伤时血脑屏障破坏导致的清蛋白渗出(P<0.05)。③黄芩苷从mRNA水平抑制脑缺血-再灌注时COX-2的诱导表达(P<0.05)。结论:黄芩苷抑制脑缺血-再灌注损伤时细胞内钙超载引起的5-LOX转位表达,从而减少cys-LT的合成,减轻血脑屏障的破坏。
Objective： To discuss the mechanism of baicalein inhibiting injury induced by focal cerebral ischemia-reperfusion in rats. Methods： The rat model of the middle cerebral artery occlusion was constructed by a standard intraluminal procedure. Changes in mRNA, COX-2 and 5-LOX related proteins were detected by RT-PCR and Western blot, the metabolites PGE2 and cys-LT evaluated by enzyme immunoassay, and the change of albumin in the brain tissues measured by SDS-PAGE. Results ： Baicalein inhibited the synthesis of cys-LT （ P 〈 0.01 ） by down-regulating cytosolic 5-LOX （ P 〈 0.01 ） , reduced the concentration of albumin in the brain homogenate （ P 〈 0.05 ） and attenuated the mRNA expression of COX-2 after cerebral ischemia-reperfusion （ P 〈 0.05 ）. Conclusion ： Baicalein could inhibit the translocation of 5-LOX induced by intracellular calcium overload following cerebral ischemia-reperfusion, and accordingly reduce the synthesis of cys-LT and attenuate the damage to the blood-brain barrier.
出处
《医学研究生学报》
CAS
2008年第6期591-593,598,共4页
Journal of Medical Postgraduates
基金
国家自然科学基金资助项目(批准号:30470604)
