Abstract Title:

Paeoniflorin attenuates cardiac dysfunction in endotoxemic mice via the inhibition of nuclear factor-κB.

Abstract Source:

Biomed Pharmacother. 2016 May ;80:200-206. Epub 2016 Mar 28. PMID: 27133057

Abstract Author(s):

Jianhua Zhai, Ying Guo

Article Affiliation:

Jianhua Zhai


The impaired cardiac function caused by reduced myocardial contractility is a typical manifestation of sepsis/septic shock. Paeoniflorin (Pae) has reportedly exhibited anti-inflammatory effect and protection against LPS-induced cardiac dysfunction in mice, but the molecular mechanism is still not fully understood. This study was designed to investigate the protective effects of Pae on lipopolysaccharide (LPS)-induced septic cardiac dysfunction and inflammation response in mice. Mice were intraperitoneal injection with Pae (15mg/kg) for 3d before the LPS challenge (10mg/kg, i.p.). Pae significantly protected against LPS-induced cardiac dysfunction and damage. Pae decreased production of inflammatory cytokines, e.g., TNF-α, IL-1β, IL-6, IL-12, MCP-1, IFN-γ, and inducible nitric oxide synthase (iNOS), in the heart of LPS-treated mice. Furthermore, Pae prevented NF-κB activation in endotoxemic mice. Pae pretreatment preserved the level of phospho-Akt. Pae effectively improved cardiac function during endotoxemia inmice. This action is attributed to Pae-induced reduction of inflammatory cytokine release and NF-κB activation, which possibly occurred via the activation PI3K/Akt signaling.

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