脂多糖
肿瘤坏死因子α
流式细胞术
NF-κB
表型
污渍
分子生物学
受体
信号转导
细胞周期
化学
细胞生物学
细胞
生物
内分泌学
生物化学
基因
作者
Li Y,Li T,Ji W,Xi Li,Yanbing Ma,Jianhua Zhao,Xuefeng Zhou
出处
期刊:PubMed
日期:2016-05-01
卷期号:32 (5): 625-9
被引量:5
摘要
To investigate the effects of pseudolaric acid B (PLAB) on the inflammatory response and M1 phenotype polarization in RAW264.7 cells induced by lipopolysaccharide (LPS) and the related mechanisms.The inflammatory model in vitro was made using RAW264.7 cells stimulated by LPS, and then was treated with 0.5 μmol/L PLAB and 1 μmol/L GW9662, a peroxisome proliferators-activated receptor γ (PPARγ) antagonist. The cell cycle was tested by flow cytometry. The mRNA expressions of PPARγ and M1 phenotype markers interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α) were measured by real-time PCR. The expression levels of signal molecules involved in nuclear factor-κB (NF-κB) signal pathway were detected by Western blotting.PLAB markedly decreased the expressions of IL-1β and TNF-α mRNAs induced by LPS and increased PPARγ mRNA level. Moreover, the expressions of NF-κB p65, pNF-κB p65, IKKα, IKKβ, pIKKα/β, IκBα and pIκBα decreased in PLAB-treated cells. Meanwhile, RAW264.7 cells were arrested in G0 and G2 phase after the treatment with PLAB. However, the effects of PLAB on RAW264.7 cells could be reversed by GW9662 obviously.PLAB could inhibit the inflammatory response and M1 phenotype polarization in RAW264.7 cells induced by LPS via modulating cell cycle and NF-κB/PPARγ signal pathway.
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