期刊
BIOMEDICINE & PHARMACOTHERAPY
卷 80, 期 -, 页码 200-206出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2016.03.032
关键词
Paeoniflorin; Cardiac dysfunction; Endotoxin; Phosphatidlyinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway
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 (15 mg/kg) for 3d before the LPS challenge (10 mg/kg, i.p.). Pae significantly protected against LPS-induced cardiac dysfunction and damage. Pae decreased production of inflammatory cytokines, e.g., TNF-alpha, IL-1 beta, IL-6, IL-12, MCP-1, IFN-gamma, and inducible nitric oxide synthase (iNOS), in the heart of LPS-treated mice. Furthermore, Pae prevented NF-kappa B activation in endotoxemic mice. Pae pretreatment preserved the level of phospho-Akt. Pae effectively improved cardiac function during endotoxemia in mice. This action is attributed to Pae-induced reduction of inflammatory cytokine release and NF-kB activation, which possibly occurred via the activation PI3K/Akt signaling. (C) 2016 Elsevier Masson SAS. All rights reserved.
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