Objectives On the basis of adriamycin (Adr)-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 Adr-induced HF were randomly divided into Adr 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 Adr group, Gs-Rb1 group and control group, in vitro. After the above intervention being performed, echoeardiography or apoptosis ratio (AR) was analysed, 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 Adr; 2. Both mRNA and protein of CX43, being significantly decreased by Adr, were significantly up-regulated by Gs-Rbl, in vivo and in vitro; 3. There was no significance for PAK1 protein between Adr 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 Adr group and in Adr group than in control group, in vivo and in vitro.
Conclusions 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.
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