首页> 中文期刊> 《中国病理生理杂志》 >罗格列酮对RAW264.7细胞源性泡沫细胞炎症反应及SOCS1和SOCS3表达的影响

罗格列酮对RAW264.7细胞源性泡沫细胞炎症反应及SOCS1和SOCS3表达的影响

         

摘要

AIM: To investigate whether perioxisome proliferator-activated receptor γ (PPAR-γ) ligand rosiglitazone regulates suppressor of cytokine signaling 1 (S0CS1) and S0CS3 expression as well as p ro - inflammatory/anti-inflammatory responses in RAW 264.7 cell-derived foam cells. METHODS: The concentrations of TNF-α, IL-6 and IL-10 in the cultured supernatant of RAW 264.7 cell-derived foam cells were detected by ELISA, and the ratios of TNF-α/IL-10 and IL-6/IL-10 were calculated. RT-PCR and Western blotting were used to analyze the effects of rosiglitazone on the expression of SOCS1 and S0CS3 at mRNA and protein levels. RESULTS: The concentrations of TNF-α, IL-6 and IL-10, and ratios of TNF-α/IL-10 and IL-6/IL-10 in foam cell group were obviously higher than those in control group, but the concentrations of the above factors in oxidized low-density lipoprotein (ox-LDL) + rosiglitazone group were apparently lower than those in foam cell group. The expression of S0CS1 and S0CS3 at mRNA and protein levels in oxLDL + rosiglitazone group was apparently higher than that in control and foam cell group. CONCLUSION: PPARγ ligand rosiglitazone up-reg-ulates the expression of SOCS1 and S0CS3 at mRNA and protein levels and regulates the balance of pro-inflammatory/anti-inflammatory responses in RAW 264.7 cell-derived foam cells.%目的:观察过氧化物酶体增殖物激活受体γ(PPARγ)配体罗格列酮是否能够调节泡沫细胞促炎/抗炎反应以及细胞因子信号抑制物1(SOCS1)和细胞因子信号抑制物3(SOCS3)的表达.方法:采用ELISA法测定泡沫细胞培养液中肿瘤坏死因子α (TNF-α)、白细胞介素(IL)-6和IL-10的水平,并计算TNF-α/IL-10和IL-6/IL-10的比值.采用RT-PCR及Western blotting技术分别观察RAW 264.7细胞源性泡沫细胞SOCS1和SOCS3 mRNA及蛋白的表达.结果:RAW 264.7细胞源性泡沫细胞组细胞培养液中TNF-α、IL-6和IL-10的水平以及TNF-α/IL-10和IL-6/IL-10的比值均明显高于对照组(control)组.而罗格列酮加入泡沫细胞培养液24 h后,TNF-α、IL-6和IL-10的浓度以及TNF-α/IL-10和IL-6/IL-10的比值均明显低于泡沫细胞组.Control组和泡沫细胞组只有少量SOCS1和SOCS3 mRNA及蛋白的表达,罗格列酮作用于泡沫细胞后SOCS1和SOCS3 mRNA及蛋白的表达均明显高于control组和氧化低密度脂蛋白(ox-LDL)组.结论:罗格列酮上调泡沫细胞SOCS1和SOCS3的表达,抑制泡沫细胞分泌TNF-α、IL-6和IL-10,调节了泡沫细胞促炎/抗炎反应.

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