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首页> 外文期刊>Cell Biology and Toxicology >The effect of activation of peroxisome proliferator-activated receptor gamma (PPAR#gamma#)on human monocyte function: PPAR#gamma# ligands do not inhibit tumor necrosis factor-#alpha# release in human monocytic cell line THP-1
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The effect of activation of peroxisome proliferator-activated receptor gamma (PPAR#gamma#)on human monocyte function: PPAR#gamma# ligands do not inhibit tumor necrosis factor-#alpha# release in human monocytic cell line THP-1

机译:过氧化物酶体增殖物激活受体γ(PPAR#gamma#)的激活对人单核细胞功能的影响:PPAR#gamma#配体不抑制人单核细胞系THP-1中的肿瘤坏死因子-αalpha#释放

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摘要

Peroxisome proliferator-activated receptor gamma (PPAR#gamma#) activation by its ligands reportedly inhibits monocyte function. However, because the concentrations of PPAR#gamma# ligands used in previous studies were higher than typically expected to activate PPAR#gamma#, we clarified whether PPAR#gamma# ligands influence monocyte function and cell viability of the human monocyte cell line THP-1. We determined tumor necrosis factor-alpha (TNF-#alpha#) release as a monocyte function and cell viability using 3-[4, 5-dimethylthiazol-2-y1]-2, 5-diphenyltetrazolium bromide. Both troglitazone and 15-deoxy-uiangle open~12, 14 -prostaglandin J_2 (15-d-PGJ2) seemed to inhibit phorbol ester-induced TNF-#alpha# release from THP-1 cells. On the other hand, neither pioglitazone nor rosiglitazone inhibited phorbol ester-induced TNF-#alpha# release. Because the cytotoxicity of troglitazone and 15-d-PGJ2 was significantly (#rho# < 0.05, Tukey-Kramer) stronger than that of pioglitazone and rosiglitazone, the inhibition of TNF-#alpha# release seemed to parallel the lack of cell viability. We concluded that PPAR#gamma# ligands did not directly inhibit TNF-#alpha# release in THP-1 cells.
机译:据报道,过氧化物酶体增殖物激活的受体γ(PPAR#gamma#)的配体激活抑制了单核细胞功能。但是,由于先前研究中使用的PPAR#gamma#配体的浓度高于通常预期的激活PPAR#gamma#的浓度,因此我们澄清了PPAR#gamma#配体是否影响人单核细胞系THP-1的单核细胞功能和细胞活力。我们确定了肿瘤坏死因子-α(TNF-α-α)释放作为单核细胞功能和细胞生存力,使用3- [4,5-二甲基噻唑-2-y1] -2,5-二苯基四唑溴化物。曲格列酮和15-脱氧核糖环打开〜12、14-前列腺素J_2(15-d-PGJ2)似乎都抑制佛波酯诱导的TNF-αα#从THP-1细胞释放。另一方面,吡格列酮和罗格列酮均未抑制佛波酯诱导的TNF-α-α释放。由于曲格列酮和15-d-PGJ2的细胞毒性显着强于吡格列酮和罗格列酮(#rho#<0.05,Tukey-Kramer),因此对TNF-#α#释放的抑制似乎与细胞活力的缺乏平行。我们得出的结论是,PPAR#γ#配体不能直接抑制THP-1细胞中TNF-#α#的释放。

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