Paeoniflorin improves myocardial injury via p38 MAPK/NF-KB p65 inhibition in lipopolysaccharide-induced mouse

Background: Paeoniflorin (Pae) is an active compound with a variety of pharmacological effects. This aim was to investigate how Pae protects against myocardial injury and to explore its potential mechanism. Methods: We established a BALB/c mouse model that was intraperitoneal injection (i.p.) of RvE1 (25 mu g/kg) or Pae (20 mg/kg) for 3 days, and then treated with lipopolysaccharide (LPS, 10 mg/kg, i.p.). The mice were randomly divided into the sham group, the LPS group, the LPS + RvE1 group, the LPS + Pae group (n=8). Cardiac dysfunction was detected by HE staining and ELISA assay. The oxidative stress, mitochondrial membrane potential (MMP), mitochondrial permeability transition pore (mPTP) and apoptosis were assessed. Furthermore, western blotting (WB) assay were employed to analyze the protective mechanisms. Results: Pae improved LPS-induced cardiac function and impeded apoptosis. Pae significantly reduced the release of inflammatory cytokines such as interleukin (IL)-6, tumor necrosis factor-alpha (TNF-alpha), and IL-1 beta. Furthermore, Pae decreased malondialdehyde (MDA), glutathione (GSH), and reactive oxygen species (ROS), and increased superoxide dismutase (SOD). In addition, Pae attenuated the mPTP opening and MMP depolarization. Notably, Pae treatment inhibited the activation of p38 MAPK and NF-Kappa B p65. Conclusions: It was confirmed that Pae alleviated LPS-induced myocardial injury. Pae might be as a new drug candidate for myocardial ischaemic complications.

Automated summary

Paeoniflorin (Pae) protects against LPS-induced myocardial injury by improving cardiac function, reducing inflammation, decreasing oxidative stress, and regulating mitochondrial function. Pae exerts its protective effects by inhibiting the activation of p38 MAPK and NF-Kappa B p65.