Effect of monosialoganglioside GM-1 on cardiopulmonary bypass-induced brain injury in rats
10.3760/cma.j.issn.0254-1416.2012.09.026
- VernacularTitle:单唾液酸神经节苷脂对体外循环诱发大鼠脑损伤的影响
- Author:
Hongqian WANG
;
Guoquan YAO
;
Yingjie SUN
;
Tiezheng ZHANG
- Publication Type:Journal Article
- Keywords:
G(M1) ganglioside;
Extracorporeal circulation;
Brain injuries
- From:
Chinese Journal of Anesthesiology
2012;(9):1122-1125
- CountryChina
- Language:Chinese
-
Abstract:
Objective 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.
