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Baicalein protects against polymicrobial sepsis-induced liver injury via inhibition of inflammation and apoptosis in mice

黄芩素 败血症 药理学 肝损伤 医学 细胞凋亡 炎症 黄芩 免疫学 细胞因子 生物 病理 中医药 生物化学 替代医学
作者
Anding Liu,Wenjie Wang,Haoshu Fang,Yan Yang,Xiaojing Jiang,Shenpei Liu,Jifa Hu,Qi Hu,Uta Dahmen,Olaf Dirsch
出处
期刊:European Journal of Pharmacology [Elsevier BV]
卷期号:748: 45-53 被引量:78
标识
DOI:10.1016/j.ejphar.2014.12.014
摘要

Liver dysfunction has been known to occur frequently in cases of sepsis. Baicalein, the main active ingredient of the Scutellaria root, exerts anti-inflammatory and anti-apoptotic properties in endotoxic shock. However, the role of baicalein in polymicrobial sepsis-induced liver injury and its regulatory mechanisms remain unclear. In this study, we aimed to investigate the protective effects of baicalein on polymicrobial sepsis-induced liver injury and to explore the possible mechanisms. Polymicrobial sepsis was induced by cecal ligation and puncture (CLP) in C57BL/6 mice. Mice were treated with baicalein (100mg/kg, i.p) at 1h, 6h and 12h following CLP. Baicalein significantly improved the survival of septic mice. Treatment with baicalein ameliorated the CLP-induced liver injury, as indicated by the lower serum aminotransferase levels and the fewer histopathologic abnormalities. Baicalein reduced the neutrophil infiltration and the hepatic inflammatory cytokine expression and release. It also decreased the hepatic and the serum high-mobility group box 1 and macrophage migration inhibitory factor levels in septic mice. Moreover, baicalein significantly inhibited the mitogen-activated protein kinases (MAPKs) activation and suppressed the transcriptional activity of nuclear factor-kappa B (NF-κB). In conclusion, these results suggest that baicalein treatment could protect against the sepsis-induced liver injury, and improve the survival of mice with polymicrobial sepsis. The mechanism of the protective action of baicalein seems to involve its ability to reduce inflammatory response, to inhibit hepatic apoptosis, and to suppress MAPKs and NF-κB activation.
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