Objectives Chronic inflammation have emerged as important role in heart failure (HF). However, suppressing local inflammatory effect of ginsenoside Rb1 (Gs-Rb1) in HF remains to be elucidated. Thus, the present study aimed at examining the effect of Gs-Rb1 in proinflammatory factor, such as tumour necrosis factor alpha (TNFα), nuclear transcription factor kappa B (NF-κB) and interleukin (IL) basing on rat HF model and cardiomyocyte insult induced by adriamycin, in vivo and ex vivo.
Methods Rat with HF and Cardiomyocytes were randomly divided into control group, HF group (i.e. adriamycin group, Gs-Rb1 group, etanercept group (soluble TNF-antagonist) and Gs-Rb1 + etanercept group. Left ventricular ejection fraction (LVEF) was estimated through echocardiographic examination and brain natriuretic peptide (BNP), the gene and the protein of proinflammatory factors through Enzyme-linked immunosorbent assay, real-time RT-PCR, Western blot and Electrophoretic mobility shift assay.
Gs-Rb1, but not etanercept, significantly improved LVEF and plasma BNP.
Gs-Rb1 markedly reduced both protein and mRNA of TNFα and TNFR-1 and augmented protein and mRNA of TNFR-2 (just in vivo), whereas etanercept almost completely eliminated TNFα protein but did not affect above other factors, in vivo and ex vivo.
Gs-Rb1 markedly inhibited IKKα phosporylation and IKKβ phosporylation induced by adriamycin, in vivo andin vitro.
Gs-Rb1 significantly caused an increase in total-IκB and a decrease in IκB phosporylation, NF-κB phosphorylation and NF-κB DNA binding activity,in vivo and ex vivo.
Gs-Rb1 significantly attenuated IL-1β concentration and markedly elevated IL-6 concentrations, in vivo and in vitro.
Conclusions The effect of Gs-Rb1, improving HF, was mediated by proinflammatory factors, including a decrease in TNFα, NF-κB, IL-1β and an increase in IL-6, in which the augment of both TNFR-2 and IκB may play a key role.