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莪术二酮通过抑制NF-κB信号通路保护脂多糖/D-半乳糖胺诱导的小鼠急性肝损伤。

Costunolide protects lipopolysaccharide/d-galactosamine-induced acute liver injury in mice by inhibiting NF-κB signaling pathway.

作者信息

Wang Yanan, Zhang Xu, Zhao Lilei, Shi Mingyu, Wei Zhengkai, Yang Zhengtao, Guo Changming, Fu Yunhe

机构信息

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, Jilin, People's Republic of China.

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, Jilin, People's Republic of China; Department of Pathogen Biology, The Key Laboratory of Zoonosis, Chinese Ministry of Education, College of Basic Medicine, Jilin University, Changchun, Jilin Province, People's Republic of China.

出版信息

J Surg Res. 2017 Dec;220:40-45. doi: 10.1016/j.jss.2017.06.083. Epub 2017 Jul 25.

Abstract

BACKGROUND

Costunolide, a well-known sesquiterpene lactone, has been reported to have anti-inflammatory and anti-oxidative effects.

METHODS

In this study, we aim to investigate the protective effects and mechanism of costunolide on lipopolysaccharide/d-galactosamine (LPS/D-Gal)-induced acute liver injury. Acute liver injury animal model was induced by intraperitoneal injection with D-Gal and LPS. Costunolide (10, 20, and 30 mg/kg) was injected intraperitoneally 1 h before or after LPS/D-Gal treatment.

RESULTS

The results showed that costunolide significantly attenuated liver pathologic changes, as well as alanine aminotransferase and aspartate aminotransferase levels in serum. Meanwhile, costunolide inhibited the expressions of interleukin (IL-1β) and tumor necrosis factor (TNF-α) in liver tissues in a dose-dependent manner. Furthermore, costunolide dose dependently inhibited LPS/D-Gal-induced NF-κB activation.

CONCLUSIONS

In conclusion, this study suggested that costunolide could attenuate LPS/D-Gal-induced liver injury and might be a potential therapeutic reagent for liver injury.

摘要

背景

木香烯内酯是一种著名的倍半萜内酯,据报道具有抗炎和抗氧化作用。

方法

在本研究中,我们旨在探讨木香烯内酯对脂多糖/d-半乳糖胺(LPS/D-Gal)诱导的急性肝损伤的保护作用及其机制。通过腹腔注射D-Gal和LPS诱导急性肝损伤动物模型。在LPS/D-Gal处理前或处理后1小时腹腔注射木香烯内酯(10、20和30mg/kg)。

结果

结果表明,木香烯内酯显著减轻了肝脏病理变化以及血清中丙氨酸氨基转移酶和天冬氨酸氨基转移酶水平。同时,木香烯内酯以剂量依赖性方式抑制肝组织中白细胞介素(IL-1β)和肿瘤坏死因子(TNF-α)的表达。此外,木香烯内酯剂量依赖性地抑制LPS/D-Gal诱导的NF-κB活化。

结论

总之,本研究表明木香烯内酯可减轻LPS/D-Gal诱导的肝损伤,可能是一种潜在的肝损伤治疗药物。

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