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香叶醇通过激活 PPARγ 来防止脂多糖和 D-半乳糖胺诱导的暴发性肝衰竭。

Geraniol protects against lipopolysaccharide and D-galactosamine-induced fulminant hepatic failure by activating PPARγ.

机构信息

Department of Infectious Diseases, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.

Department of Pathophysiology, School of Basic Medical Science Central South University, Changsha, Hunan, 410083, China.

出版信息

Microb Pathog. 2019 Mar;128:7-12. doi: 10.1016/j.micpath.2018.11.054. Epub 2018 Dec 11.

Abstract

Geraniol (GOH), a natural component of plant essential oils, exhibits potent antioxidant and anti-inflammatory properties. The aim of this study was to assess the protective effects and mechanisms of GOH on lipopolysaccharide (LPS)/d-galactosamine (D-GalN)-induced fulminant hepatic failure (FHF). Mice were treated with GOH (12.5, 25, and 50 μg/kg) 1 h before challenging LPS (60 mg/kg) and D-GalN (800 mg/kg). 8 h later LPS/D-GlaN treatment, mice were sacrificed and the serum and the liver tissues were collected for testing. The liver pathological changes were assessed by H & E staining. MPO activity, MDA level in liver tissues, and AST, ALT levels in serum were detected by specific detection kits. The levels of TNF-α and IL-1β were detected by ELISA. The expression of NF-κB and PPARγ were detected by western blot analysis and qRT-PCR. The results showed that GOH had a protective effect on LPS/D-GalN-induced FHF, as evidence by the attenuation of liver pathological injury, MPO activity, MDA level, and serum AST and ALT levels. GOH reduced liver TNF-α and IL-1β levels through inhibiting NF-κB signaling pathway activation. Furthermore, GOH increased PPARγ expression in FHF induced by LPS/D-GalN. In conclusion, the present study proved that GOH protects against LPS/D-GalN-induced FHF through inhibiting inflammatory response and increasing PPARγ expression.

摘要

香叶醇(GOH)是植物精油的一种天然成分,具有很强的抗氧化和抗炎特性。本研究旨在评估 GOH 对脂多糖(LPS)/D-半乳糖胺(D-GalN)诱导的暴发性肝衰竭(FHF)的保护作用和机制。小鼠在接受 LPS(60mg/kg)和 D-GalN(800mg/kg)攻击前 1 小时用 GOH(12.5、25 和 50μg/kg)处理。在 LPS/D-GlaN 处理 8 小时后,处死小鼠并收集血清和肝脏组织进行检测。通过 H&E 染色评估肝脏病理变化。通过特定检测试剂盒检测肝组织中 MPO 活性、MDA 水平以及血清中 AST、ALT 水平。通过 ELISA 检测 TNF-α和 IL-1β水平。通过 Western blot 分析和 qRT-PCR 检测 NF-κB 和 PPARγ的表达。结果表明,GOH 对 LPS/D-GalN 诱导的 FHF 具有保护作用,表现在肝病理损伤、MPO 活性、MDA 水平以及血清 AST 和 ALT 水平的减轻。GOH 通过抑制 NF-κB 信号通路的激活降低了肝 TNF-α和 IL-1β水平。此外,GOH 增加了 LPS/D-GalN 诱导的 FHF 中 PPARγ的表达。综上所述,本研究证明 GOH 通过抑制炎症反应和增加 PPARγ表达来保护 LPS/D-GalN 诱导的 FHF。

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