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

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• 作者：Jianhua Zhai^a ; ¹ ; ^{ZhaiJianhua2015@163.com" class="auth_mail" title="E-mail the corresponding author} ; Ying Guo^b ; ¹
• 关键词：Paeoniflorin ; Cardiac dysfunction ; Endotoxin ; Phosphatidlyinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway
• 刊名：Biomedicine & Pharmacotherapy
• 出版年：2016
• 出版时间：May 2016
• 年：2016
• 卷：80
• 期：Complete
• 页码：200-206
• 全文大小：1960 K

文摘

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-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 in mice. 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.