人参皂苷Rbl对阿霉素心力衰竭大鼠心肌细胞核因子-κB的影响

目的探讨人参皂苷Rbl(Gs-Rb1)改善阿霉素(Adr)慢性心力衰竭(CHF)效应是否与抑制核因子-κB(NF-κB)有关。方法 Adr诱导CHF大鼠模型被随机分为Adr组(n=15)和Gs-Rbl组(70 mg.kg-1.d-1,n=17),另随机选取同龄健康大鼠作为对照(n=10);同时培养乳鼠心肌细胞并随机分为对照组、Adr组(1μmol.L-1)和Gs-Rbl组(1μmol.L-1Adr+200μmol.L-1 Gs-Rbl)。干预完毕后,检测心脏超声、NF-κB、IκBα、p-IκBα和NF-κB DNA结合活性。结果 (1)Gs-Rb1组LVEF明显改善(P=0.003);(2)在NF-κB p50和NF-κB p65方面,体内或体外的Gs-Rbl组均明显低于Adr组(P<0.001);(3)体内、体外的Gs-Rbl组NF-κBDNA结合活性明显低于Adr组(P<0.01);(4)体内、体外的Adr组IκBα蛋白明显高于对照组,而Gs-Rbl组IκBα最高(P<0.01);Gs-Rbl组p-IκBα和p-IκBα/IκBα比值明显低于Adr组(P<0.01)。结论 Gs-Rb1改善CHF效应与其抑制NF-κB活性有关。

Effects of Ginsenosides-Rbl on nuclear factor kappa B in rats with chronic heart failure induced by adriamycin

Aim Based on the adriamycin(Adr)-induced chronic heart failure(CHF),the present study elucidates the effect of Ginsenosides-Rbl(Gs-Rb1) on nuclear factor kappa B(NF-κB),in vivo and in vitro.Methods CHF rats were randomly divided into Adr group(n=15) and Gs-Rb1 group(70 mg·kg-1·d-1,n=17),and the age-matched rats as control(n=15);in addition,cardiomyocytes were randomly divided into control group,Adr group(1 μmol·L-1) and Gs-Rb1 group(1 μmol·L-1 Adr+200 μmol·L-1 Gs-Rb1),too.After the above intervention was performed,the left ventricular ejection fraction(LVEF) was analyzed by echocardiography,in vivo,the expression of NF-κB,IκBα,p-IκBα and NF-κB DNA binding activity were assayed.Results(1) LVEF was significantly improved in Gs-Rb1 group than in Adr group(P=0.003).(2) Both NF-κB p50 and NF-κB p65 were significantly down-regulated in Gs-Rb1 group than in Adr group(P<0.01),in vivo and ex vivo.(3) NF-κB DNA binding activity was significantly down-regulated in Gs-Rb1 group than in Adr group(P<0.01),in vivo and ex vivo.(4) IκBα protein was significantly up-regulated by Adr,especially by Gs-Rb1,compared with control(P<0.01),in vivo and in vitro;both p-IκBα protein and p-IκBα/IκBα ratio were significantly lower in Gs-Rb1 group than in Adr group,in vivo and in vitro.Conclusion The effects of Gs-Rb1 on the improvement of CHF were partly performed by means of inhibiting NF-κB at least.