CAJ | 학술논문

目的评价单唾液酸神经节苷脂(GM1)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 ～ 450 g,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+ GM1组(G组).G组在预充液中加入GM1 20 mg/kg;C组预充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-100β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Western blot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-100β蛋白、TNF-α和IL-6浓度升高,海马MMP-9表达上调,NF-κB活性增强,IL-10表达下调(P＜0.05)；与CPB组比较,G组血浆NSE、S-100β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.
목적 평개단타액산신경절감지(GM1)대체외순배(CPB)대서염성반응적영향.방법 성년웅성SD대서24지,체중350 ～ 450 g,4～6월령,채용수궤수자표법,장기분위3조(n=8):가수술조(S조)、CPB조、CPB+ GM1조(G조).G조재예충액중가입GM1 20 mg/kg;C조예충액중가입등용량생리염수.CPB조화G조우CPB정지후3h시,S조우상응시점,취경정맥혈양,채용ELISA법측정혈장신경원특이성희순화매(NSE)화S-100β단백농도,채용방사면역분석법측정혈장TNF-α화IL-6농도；취해마조직,채용Western blot법검측해마기질금속단백매-9(MMP-9)、IL-10표체급NF-κB활성.결과 여S조비교,CPB조화G조혈장NSE、S-100β단백、TNF-α화IL-6농도승고,해마MMP-9표체상조,NF-κB활성증강,IL-10표체하조(P＜0.05)；여CPB조비교,G조혈장NSE、S-100β단백、TNF-α화IL-6농도강저,해마MMP-9표체하조,NF-κB활성감약,IL-10표체상조(P＜0.05).결론 GM1감경CPB유발대서뇌손상적궤제가능여억제중추화전신염성반응유관.
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.