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Fraxin inhibits lipopolysaccharide‐induced inflammatory cytokines and protects against endotoxic shock in mice
Author(s) -
Li Weifeng,
Li Wenqi,
Yu JinJin,
Liu Fang,
Zang Lulu,
Xiao Xin,
Zhao Jinmeng,
Yao Qing,
Niu Xiaofeng
Publication year - 2020
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/fcp.12500
Subject(s) - lipopolysaccharide , tumor necrosis factor alpha , western blot , nitric oxide , aspartate transaminase , inflammation , pharmacology , alanine transaminase , interleukin , nitric oxide synthase , immunology , nf κb , chemistry , cytokine , medicine , biology , biochemistry , alkaline phosphatase , enzyme , gene
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.