Suppressing Local Inflammatory Effect of Ginsenoside Rb1 in Adriamycin-Induced Cardiomyocyte Injury

The aim of this study is to elucidate the anti-inflammation effect of ginsenoside Rb1 (Gs-Rb1) on heart failure (HF). Those factors mainly include tumor necrosis factor alpha (TNF alpha), nuclear transcription factor kappa B (NF-kappa B), interleukin (IL) and so on. Rats or cardiomyocytes were randomly divided into control group, HF group (adriamycin group), Gs-Rb1 group, etanercept group (soluble TNF-antagonist), and-Gs-Rb1 + etanercept group, respectively. Left ventricular ejection fraction. (LVEF) and brain natriuretic peptide (BNP) were estimated, and the proinflammatory factors were assayed through enzyme-linked immunosorbent assay, real-time RT-PCR, Western blot and electrophoretic mobility shift assay, respectively. Gs-Rb1, but not etanercept, significantly improved LVEF and markedly decreased plasma BNP. Gs-Rb1 markedly reduced both protein and mRNA of TNF alpha and TNFR-1, and augmented protein and mRNA of TNFR-2 (just in vivo); in addition, etanercept almost completely eliminated TNFa protein but did not affect above other factors, in vivo and ex vivo. Gs-Rb1 markedly inhibited IKK beta phosporylation and IKK beta phosporylation induced by adriamycin, in vivo and in vitro. Gs-Rb1 significantly caused an increase in total-I kappa B and a decrease in I kappa B phosporylation, NF-kappa B phosphorylation and NF-kappa B DNA binding activity, in vivo and ex vivo. Gs-Rb1 significantly attenuated IL-1 beta and markedly elevated IL-6, in vivo and in vitro. The effect of Gs-Rbl, improving HF, was mediated by adjusting pro-inflammatory factors, including a decrease in TNF alpha, NF-kappa B, IL-1 beta and an increase in IL-6, in which TNFR-2 and kappa B may play a key role.