Paeoniflorin improves pressure overload-induced cardiac remodeling by modulating the MAPK signaling pathway in spontaneously hypertensive rats.

Paeoniflorin (PF) is a main bioactive component of the root of Paeonia lactiflora Pal, and previous investigations suggest that it may impact cardiac remodeling in spontaneous hypertensive rats (SHR) via the MAPK signaling pathway. Thus, the purpose of this investigation was to examine the impacts of paeoniflorin cardiac function in SHR rats. Cardiac function and blood pressure were observed using echocardiography and non-invasive tail pressure gauge. Heart histopathology was assessed by histological staining and transmission electron microscopy. Genomic sequencing was performed and signaling pathway enrichment analyzed the function of differentially expressed genes(DEGs). Biochemical kits were used to analyze the serum level of proinflammatory cytokines including TNF-α, IL-6 and MCP-1. qRT-PCR proved the mRNA expression of Ngfr, Grin2b, and Ntf4. MAPK pathways were determined via western blot. Paeoniflorin decreased blood pressure and increased hemodynamic indexes. 131 DEGs were identified (SHR vs. PF), and mainly enriched on the MAPK signaling pathway. Paeoniflorin reduced IL-6, MCP-1, Ngfr, Grin2b, and Ntf4, and also decreased p-JNK, p-Erk1/2, and p-p38 proteins compared with the SHR group. Paeoniflorin attenuated cardiac hypertrophy, cardiac fibrosis, and inflammation, and subsequently improved LV function. In conclusion, the cardioprotective role of paeoniflorin was associated with the inhibition of MAPK signaling pathway.