Protective effects of β-eudesmol against septic liver injury via inhibition of NF-KB signaling

被引:5
|
作者
Xu, Qigang [1 ]
Li, Junjian [1 ]
Chen, Zhe [1 ]
Mao, Yefan [1 ]
Tao, Chonglin [1 ]
机构
[1] Wenzhou Med Univ, Affiliated Hosp 1, Dept Hepatobiliary Pancreat Surg, Wenzhou 325015, Zhejiang, Peoples R China
关键词
fi-Eudesmol; Inflammation; Oxidative stress; Cecal ligation and puncture; Sepsis; Liver injury; NF-KB; ACUTE KIDNEY INJURY;
D O I
10.4314/tjpr.v21i6.7
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Purpose: To investigate the role of fi-eudesmol in septic liver injury in mice. Methods: Mice were intraperitoneally injected with 50 or 100 mg/kg fi-eudesmol, and then subjected to cecal ligation and puncture for the establishment of a septic model 2 h later. Haematoxylin and eosin staining was used to evaluate histopathological changes in the liver tissues. Terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) staining and enzyme-linked immunosorbent assay (ELISA) were employed to determine liver damage, while inflammation and oxidative stress were evaluated by ELISA. Results: Liver tissues of septic mice showed infiltration of inflammatory cells, vacuolar degeneration and obscure nucleus. However, treatment with fi-eudesmol ameliorated the histopathological changes (p < 0.01). Moreover, fi-eudesmol also reduced hepatocyte apoptosis, and decreased the levels of biomarkers for liver damage. The up-regulation of TNF-a, IL-1fi, IL-6 in septic mice were significantly down-regulated by fi-eudesmol (p < 0.01), but increased the levels of superoxide dismutase (SOD) and glutathione (GSH) and decreased malondialdehyde (MDA) and myeloperoxidase (MPO) in order to protect the mice against sepsis. In addition, fi-eudesmol attenuated the cecal ligation and puncture-induced up-regulation of p-p65 in mice (p < 0.01). Conclusion: fi-Eudesmol exerts anti-inflammatory and anti-oxidant effects in septic mice by inactivating NF-KB signaling, and thus may be useful as a potential agent in the management of sepsis.
引用
收藏
页码:1183 / 1188
页数:6
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