Objectives Basing on the adriamycin-induced chronic heart failure (CHF), the present study elucidated whether the effect of Ginsenosides-Rbl (Gs-Rb1) improving cardiac function was performed by inhibiting nuclear factor kappa B (NF-κB), in vivo and in vitro.

Methods CHF models of rats were performed by adriamycin, in vito, and the neonatal rat cardiomyocytes were cultured, ex vivo. Then CHF rats were randomly divided into control group (n = 15), adriamycin group (n = 15) and Gs-Rb1 group (70 mg/kg·d, n = 17), and cells randomly divided into control group, adriamycin group (1 umol/L) and Gs-Rb1 group (200 uMol/L), too. After the intervention being performed, the left ventricular ejection fraction (LVEF) was analysed by echoeardiography, the expression of NF-κB, IκBα, p-IκBα and NF-κB DNA binding activity were assayed.

Results 1. Left ventricular ejection fraction (LVEF) was significantly improved in Gs-Rb1 group than in adriamycin group (P = 0.003). 2. Both protein of NF-κB p50 and NF-κB p65 were significantly up-regulated in adriamycin group than in control group (P < 0.01), and significantly down-regulated in Gs-Rb1 group than in adriamycin group, in vivo and ex vivo. 3. NF-κB DNA binding activity was significantly up-regulated in adriamycin group than in control group, which were significantly down-regulated in Gs-Rb1 group than in adriamycin group. 4. IκBα protein was significantly up-regulated by adriamycin, especially by Gs-Rb1, compared to control; IκBα significantly down-regulated in Gs-Rb1 group than in adriamycin group, in vivo and in vitro. Both p-IκBα protein and p-IκBα/IκBα ratio were significantly higher in adriamycin group than in control group, both of which were significantly lower in Gs-Rb1 group than in adriamycin group, in vivo and in vitro.

Conclusions The effects of Gs-Rb1, relieving CHF, were partly performed by means of adjusting NF-κB at least.