大黄素
NF-κB
肿瘤坏死因子α
促炎细胞因子
细胞因子
免疫印迹
IκB激酶
炎症
生物
细胞生物学
癌症研究
分子生物学
化学
免疫学
生物化学
基因
作者
Hailong Li,Hailong Chen,Hong Li,Kaili Zhang,Xiaoyan Chen,Xiaowei Wang,Qing‐You Kong,Jia Liu
摘要
Emodin, an anthraquinones component of Rheum palmatun, has been used for anti-inflammatory purposes. However, its underlying molecular effect(s) on target cells remain to be well clarified. Thus, our current study was aimed at investigating the regulatory mechanism of emodin on liposaccharide-induced inflammatory responses in RAW 264.7 macrophages by RT-PCR, Western blot analysis, immunocytochemical staining and immunofluorescence analysis. It was found that a treatment of 20 microg/ml emodin inhibited the expression of a panel of inflammatory-associated genes, including TNFalpha, iNOS, IL-10, cytosolic IkappaBalpha, IKK-alpha and IKK-gamma, to different extents as well as the nuclear translocation of NF-kappaB (nuclear factor-kappaB). The promoting effect of emodin on the production and translocation of p105 (the precursor of NF-kappaB p50) was time-dependent and reached a maximum at 5 h. Our data suggest that emodin plays its anti-inflammatory roles by regulating inflammatory cytokines, specifically by suppressing NF-kappaB activation.
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