脂多糖
肿瘤坏死因子α
污渍
炎症
化学
NF-κB
一氧化氮合酶
αBκ
过氧化物酶体增殖物激活受体
基因敲除
一氧化氮
促炎细胞因子
药理学
分子生物学
信号转导
生物化学
生物
受体
免疫学
细胞凋亡
基因
有机化学
作者
Quan Wen,Liyan Mei,Sen Ye,Xia Liu,Qin Xu,Jiahao Miao,Shisuo Du,Dongfeng Chen,Chun Li,Hui Li
标识
DOI:10.1016/j.intimp.2018.01.023
摘要
Sepsis is a life-threatening disease. Inflammation is a major concomitant symptom of sepsis Chrysophanol, an anthraquinone derivative isolated from the rhizomes of rheumpalmatum, has been reported to have a protective effect against lipopolysaccharide(LPS)-induced inflammation. However, the underlying molecular mechanisms are not well understood. The aim of this study was to explore the effect and mechanism of chrysophanol on lipopolysaccharide (LPS)-induced anti-inflammatory effect of RAW264.7 cells and its involved potential mechanism. The mRNA and protein expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and inducible nitric oxide synthase (iNOS), nuclear factor kappa B (NF-κB) and PPAR-γ were measured by qRT-PCR and western blotting, the production of TNF-α, IL-1β was evaluated by ELISA. Then, the phosphorylation of NF-κB p65 was also detected by western blotting. And NF-κB p65 promoter activity was analyzed by the Dual-Luciferase reporter assay system as well. Meanwhile, PPAR-γ inhibitor GW9662 was performed to knockdown PPAR-γ expression in cells. Our data revealed that LPS induced the up-regulation of TNF-α, IL-1β, iNOS and NF-κB p65, the down-regulation of PPAR-γ were substantially suppressed by chrysophanol in RAW264.7 cells. Furthermore, our data also figured out that these effects of chrysophanol were largely abrogated by PPAR-γ inhibitor GW9662. Taken together, our results indicated that LPS-induced inflammation was potently compromised by chrysophanol very likely through the PPAR-γ-dependent inactivation of NF-κB in RAW264.7 cells.
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