单唾液酸神经节苷脂对体外循环大鼠炎性反应的影响

Effect of monosialoganglioside GM1 on cardiopulmonary bypass-induced inflammatory response in rats

目的评价单唾液酸神经节苷脂（GMI）对体外循环（CPB）大鼠炎性反应的影响。方法成年雄性SD大鼠24只，体重350～450g，4～6月龄，采用随机数字表法，将其分为3组（n=8）：假手术组（S组）、CPB组、CPB＋GMI组（G组）。G组在预充液中加入GMI20mg／kg；C组预允液中加入等容量生理盐水。CPB组和G组于CPB停止后3h时，S组于相应时点，取颈静脉血样，采用ELISA法测定血浆神经元特异性烯醇化酶（NSE）和S-10013蛋白浓度，采用放射免疫分析法测定血浆TNF-α和IL-6浓度；取海马组织，采用Westernblot法检测海马基质金属蛋白酶．9（MMP-9）、IL-10表达及NF-κB活性。结果与S组比较，CPB组和G组血浆NSE、S-1008蛋白、TNF—α和IL-6浓度升高，海马MMP-9表达上调，NF-vB活性增强，IL-10表达下调（P〈0．05）；与CPB组比较，G组血浆NSE、S-100p蛋白、TNF-α和IL-6浓度降低，海马MMP-9表达下调，NF—κB活性减弱，IL-10表达上调（P〈0．05）。结论GM1减轻CPB诱发大鼠脑损伤的机制可能与抑制中枢和全身炎性反应有关。

Objective To investigate the effect of monosialoganglioside GMI 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 ＋ GM1 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 hipp-ocampi were isolated to detect the expression of hippocampal matrix metalloproteinase-9 （MMP-9） and IL-10 and NF-κB activity in hippoc＇ampal 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-IOOp 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.