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Blockage of PPARδ increases the expression of inflammatory factors in 3T3-L1 cells stimulated with TNFα

机译:PPARδ的阻滞增加了TNFα刺激的3T3-L1细胞中炎性因子的表达

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Objective: To investigate the role of peroxisome proliferator-activated receptors δ (PPARδ) in inflammatory reaction and its possible mechanism in adipocyte. Methods :Lentivirus-mediated RNA interference (RNAi) was used to block the expression of PPARδ in 3T3-L1 cells. In order to induce inflammation in 3T3-L1, cells were stimulated with tumor necrosis factor-α(TNFα, 20 ng/ml) for 4 h. The expression of PPARδ, nuclear factor κB (NFκB) and C reactive protein (CRP) were determined by Western blot analysis. Results: The expression of PPARδ was reduced by 80% after RNAi. Blockage of PPARδ promoted the expression of CRP and NFκB in cells stimulated with TNFα, but had no effect on normal cells. Conclusion: PPARδ is involved in inflammatory reaction in adipocyte. Blockage of PPARδ can promote the inflammation mediated by inflammatory factors and increase the expression of NFκB and CRP in 3T3-L1 cells stimulated with TNFα.
机译:目的:探讨过氧化物酶体增殖物激活受体δ(PPARδ)在炎症反应中的作用及其在脂肪细胞中的可能机制。方法:用慢病毒介导的RNA干扰(RNAi)阻断3T3-L1细胞中PPARδ的表达。为了诱导3T3-L1发炎,用肿瘤坏死因子-α(TNFα,20ng / ml)刺激细胞4小时。 Western blot分析检测PPARδ,核因子κB(NFκB)和C反应蛋白(CRP)的表达。结果:RNAi后PPARδ的表达降低了80%。 PPARδ的阻断促进了TNFα刺激的细胞中CRP和NFκB的表达,但对正常细胞没有影响。结论:PPARδ参与脂肪细胞的炎症反应。 PPARδ的阻断可促进炎症因子介导的炎症,并增加TNFα刺激的3T3-L1细胞中NFκB和CRP的表达。

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