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牡荆素抑制脂多糖诱导的炎症细胞因子,防止内毒素休克的发生。

Fraxin inhibits lipopolysaccharide-induced inflammatory cytokines and protects against endotoxic shock in mice.

机构信息

School of Pharmacy, Xi'an Jiaotong University, Xi'an, 710061, China.

Key Laboratory of Material Basis Analysis of Chinese Medicine, Shaanxi Administration of Traditional Chinese Medicine, Xi'an, 710061, China.

出版信息

Fundam Clin Pharmacol. 2020 Feb;34(1):91-101. doi: 10.1111/fcp.12500. Epub 2019 Aug 28.

DOI:10.1111/fcp.12500
PMID:31325387
Abstract

Fraxin, the effective component isolated from Cortex Fraxini, has been reported to have anti-inflammation effects. The aim of this study was to explore the effect of fraxin on lipopolysaccharide (LPS)-induced endotoxic shock in mice. We used Kunming male mice to establish the model, and we found that fraxin could improve the survival rate of the LPS-induced mice. Histopathological study showed that fraxin could mitigate the injuries in LPS-induced lung and liver tissues. The levels of tumour necrosis factor-α and interleukin-6 both in serum and lung, liver tissues, and the productions of nitric oxide (NO), aspartate transaminase and alanine transaminase in serum were decreased by fraxin. Western blot assay demonstrated that the pretreatment with fraxin could downregulate LPS-induced protein expressions of nuclear factor-kappa B (NF-κB) and NLRP3 inflammatory corpuscle signalling pathways. Overall, fraxin had protective effects on LPS-induced endotoxic shock mice and the possible mechanisms might activate through NF-κB and NLRP3 inflammatory corpuscle signalling pathways.

摘要

秦皮素是从秦皮中分离得到的有效成分,具有抗炎作用。本研究旨在探讨秦皮素对脂多糖(LPS)诱导的内毒素休克小鼠的作用。我们使用昆明雄性小鼠建立模型,发现秦皮素可以提高 LPS 诱导的小鼠的存活率。组织病理学研究表明,秦皮素可以减轻 LPS 诱导的肺和肝组织损伤。秦皮素还降低了血清和肺、肝组织中肿瘤坏死因子-α和白细胞介素-6 的水平,以及血清中一氧化氮(NO)、天门冬氨酸转氨酶和丙氨酸转氨酶的产生。Western blot 分析表明,秦皮素预处理可以下调 LPS 诱导的核因子-κB(NF-κB)和 NLRP3 炎性小体信号通路的蛋白表达。总之,秦皮素对 LPS 诱导的内毒素休克小鼠具有保护作用,其可能的机制是通过 NF-κB 和 NLRP3 炎性小体信号通路激活。

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