Abstract: Objective    On the basis of doxorubicin(Dox)-induced heart failure (HF), the present study elucidated whether the effect of Ginsenosides-Rbl (Gs-Rb1), improving cardiac function, was performed by connexin 43 (CX43) and other mechanisms. Methods    Rats with Dox-induced HF were randomly divided into Dox group (n=15) and Gs-Rb1 group (n=17), and the health age-matched rat was as control (n=15); In addition, cardiomyocytes was randomly divided into Dox group, Gs-Rb1 group and control group, in vitro. After the above intervention being performed, echoeardiography or apoptosis ratio (AR) was analyzed, respectively. CX43, p21-activated kinase 1 (PAK2) and protein phosphatase type 2A (PP2A) was assayed by western bolt or Rt-PCR, respectively. Results    1. Gs-Rbl significantly improved LVEF (in vivo), markedly left ventricular weight index (in vivo) and significantly inhibited cell apoptosis (in vitro), all of which were induced by Dox; 2. Both mRNA and protein of CX43, being significantly decreased by Dox, were significantly up-regulated by Gs-Rbl, in vivo and in vitro; 3. There was no significance for PAK1 protein between Dox group and control group, which was markedly increased by Gs-Rbl, in vivo and in vitro; 4. PP2A protein was significantly up-regulated in Gs-Rbl group than in Dox group and in Dox group than in control group, in vivo and in vitro. Conclusion   The effect of Gs-Rb1, improving HF and inhibiting cell apoptosis, was partly performed through adjusting CX43 at least, which may be mediated by PAK1-PP2A.

Key words: Ginsenosides-Rbl, connexin 43, myocardium, p21-activated kinase 1, protein phosphatase type 2A