败血症
化学
免疫学
NF-κB
p38丝裂原活化蛋白激酶
肿瘤坏死因子α
炎症
先天免疫系统
免疫印迹
信号转导
药理学
免疫系统
分子生物学
生物
MAPK/ERK通路
生物化学
基因
作者
Zhelong Nie,Jia Li,Yang Zhao,Sheng Zhang,Yanwei Zhang,Junhui Wang
标识
DOI:10.1016/j.bmc.2020.115945
摘要
Sepsis is a severe systemic inflammatory response induced by infection. Innate immunity recognizes pathogen components such as lipopolysaccharides (LPS), and mediates the polarization of immune cells and the release of cytokines. However, this process is also crucial for triggering sepsis and septic shock. To investigate the potential therapeutic function of 11H-indeno [1,2–b] quinoxalin-11-one oxime (IQ-1S) to sepsis, LPS plus d-galactosamine was used to establish a sepsis mouse model. Flow cytometry was performed to catalyze T cells and macrophages in mouse spleen. ELISA assay and qRT-PCR assay were performed to estimate the expression levels of cytokines and related genes including TNF-α, IL-6, IL-1β, Nos2, Arg and Mrc. The protein levels of NF-κB, AP1, NF-Y, p-JNK2, JNK2, p-p38, p38, p-IκBα, IκBα, p-IKKβ and IKKβ were evaluated by Western blot assay. IQ-1S treatment significantly reduced mortality and lung inflammation in sepsis mice. IQ-1S treatment decreased the levels of inflammatory cytokines in sepsis mice. Polarization of M1 macrophages was suppressed by IQ-1S in vitro. IQ-1S significantly inhibited the activation of the JNK signaling pathway and reduced the phosphorylation level of JNK2 in sepsis mice. IQ-1S protected the mice against LPS-induced sepsis through inhibiting JNK signaling pathway.
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