Effect of monosialoganglioside GM1 on cardiopulmonary bypass-induced inflammatory response in rats
10.3760/cma.j.issn.0254-1416.2013.01.033
- VernacularTitle:单唾液酸神经节苷脂对体外循环大鼠炎性反应的影响
- Author:
Huijuan CAO
;
Zhen ZHANG
;
Tiezheng ZHANG
;
Hongqian WANG
;
Jin ZHOU
;
Jing YAO
- Publication Type:Journal Article
- Keywords:
G(M1) Ganglioside;
Extracorporeal circulation;
Brain injuries;
Systemic inflammatory response syndrome
- From:
Chinese Journal of Anesthesiology
2013;(1):119-122
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of monosialoganglioside GM1 on cardiopulmonary bypass (CPB)-induced inflammatory response in rats.Methods Twenty-four adult male Sprague-Dawley rats,weighing 350-450 g,were randomly divided into 3 groups (n =8 each):sham operation group (group S),group CPB and CPB + GMi group (group G).GM1 20 mg/kg was added to the priming solution in group G.While the equal volume of normal saline was given in group CPB.Blood samples were collected from the jugular vein at 3 h after termination of CPB for determination of plasma concentrations of neuron-specific enolase (NSE) and S-100β protein (by ELISA) and tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) (by radioimmunoassay).The hippocampi were isolated to detect the expression of hippocampal matrix metalloproteinase-9 (MMP-9) and IL-10 and NF-κB activity in hippocampal tissues by Western blot.Results Compared with group S,the plasma concentrations of NSE,S-100β protein,TNF-α and IL-6 and NF-κB activity were significantly increased,the expression of MMP-9 was up-regulated,and the expression of IL-10 was down-regulated in groups CPB and G (P ＜ 0.05).Compared with group CPB,the plasma concentrations of NSE,S-100β protein,TNF-α and IL-6 and NF-κB activity were significantly decreased,the expression of MMP-9 was down-regulated,and the expression of IL-10 was upregulated in group G (P ＜ 0.05).Conclusion The mechanism by which GM1 reduces the CPB-induced brain damage may be related to reduction of the central and systemic inflammatory response in rats.
