摘要目的 评价单唾液酸神经节苷脂(GM-1)对体外循环(CPB)诱发大鼠脑损伤的影响.方法 成年雄性SD大鼠27只,15月龄,体重350～ 450 g.采用随机数字表法,将大鼠随机分为3组(n=9):对照组(C组)、CPB组和GM-1组.采用右颈静脉腔房引流,右颈动脉灌注法建立大鼠CPB模型.CPB组和GM-1组行CPB 1 h,其中GM-1组预充液中加入GM-1 20 mg/kg,CPB组给予等容量的生理盐水.CPB结束后3h和C组机械通气结束后3h时断头取左侧脑组织,透射电镜下观察海马超微结构变化;TUNEL法检测海马神经元调亡情况;免疫组化和Western blot法检测Bax和Bcl-2蛋白表达水平.结果 与C组比较,CPB组和GM-1组凋亡神经元增多,Bax和Bcl-2蛋白表达上调,Bax/Bcl-2比值升高(P＜0.05);与CPB组比较,GM-1组凋亡神经元减少,Bax蛋白表达下调,Bcl-2蛋白表达上调,Bax/Bcl-2比值降低(P＜0.05).CPB组海马神经元病理损伤严重,GM-1组海马神经元病理损伤减轻.结论 GM-1可减轻CPB诱发大鼠脑损伤,其机制可能与其抑制神经元凋亡有关.

abstractsObjective To investigate the effect of monosialoganglioside GM-1 on cardiopulmonary bypass (CPB)-induced brain injury in rats.Methods Twenty-seven adult male Sprague-Dawley rats,weighing 350-450 g,aged 15 months,were randomly divided into 3 groups (n=9 each): control group (C group),CPB group and GM-1 group.The animals were anesthetized with chloral hydrate,tracheostomized and mechanically ventilated.Right common carotid and right jugular vein were cannulated for closed-chest CPB.In groups CPB and GM-1,the rats underwent 1 h CPB.GM-1 20 mg/kg was added to the priming solution in group GM-1,while the equal volume of normal saline was given in group CPB.The animals were sacrificed at 3 h after termination of CPB or 3 h after the end of ventilation in group C,the brains were removed and the hippocampi isolated for microscopic examination and for determination of apoptosis (using TUNEL) and Bax and Bcl-2 protein expression (by immunohistochemistry and Western blot).Results Compared with group C,the number of apoptotic neurons and ratio of Bax/Bcl-2 were significantly increased,and the expression of Bcl-2 and Bax protein was up-regulated in groups CPB and GM-1 (P ＜ 0.05).Compared with group CPB,the number of apoptotic neurons and ratio of Bax/Bcl-2 were significantly decreased,the expression of Bax protein was down-regulated and the expression of Bcl-2 protein was up-regulated in group GM-1.The pathological changes were severe in group CPB and attenuated in group GM-1.Conclusion GM-1 can attenuate CPB-induced brain injury in rats and inhibition of the apoptosis in neurons may be involved in the mechanism.