Objectives Basing on the adriamycin-induced heart failure (HF), the present study elucidated whether the effect of Ginsenosides-Rbl (Gs-Rb1) improving cardiac function was performed by inhibiting protein kinase R-like ER kinase (PERK) pathway.
Methods Adriamycin-induced rats with HF were randomly divided intoHF group (n = 15) and Gs-Rb1 group (n = 17), and the health age-matched rat was as control (n = 15). After the intervention being performed and the left ventricular ejection fraction (LVEF) was analysed by echoeardiography, glucose-regulated protein 78 (GRP78), protein kinase R-like ER kinase (PERK), p-PERK, eukaryotic initiation factor 2α (eIF2α), p-eIF2α, C/EBP homologous protein (CHOP) and caspase-12 were assayed by western bolt and Rt-PCR.
HF was performed by adriamycin, LVEF was significantly improved by Gs-Rb1 (P = 0.000).
Both mRNA and protein of GRP78 were significantly up-regulated in HF group than in control group (P = 0.000), which were significantly down-regulated in Gs-Rb1 group than in HF group (P = 0.000).
Both PERK and p-PERK were significantly inhibited by Gs-Rb1, compared to HF group (P = 0.000).
eIF2α mRNA, eIF2α protein and p-eIF2α protein, being significantly up-regulated by adriamycin, were markedly down-regulated by Gs-Rb1.
Both mRNA and protein of CHOP were significantly higher in HF group than in control group (P = 0.000), which were significantly lower in Gs-Rb1 group than in HF group (P = 0.000).
Both mRNA and protein of caspase-12, being significantly increased in HF group (P = 0.000), were markedly decreased by Gs-Rb1 (P = 0.000).
Conclusions The effect of Gs-Rb1, improving HF, was partly fulfilled through adjusting PERK pathway at least.