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目的 :研究过氧化酶体增殖物激活型受体 (PPAR)γ对人类单核或巨噬细胞核因子抑制蛋白 (IkBα)和基质金属蛋白酶 1 (MMP 1 )表达的调控影响 ,探讨PPARγ在抑制炎症反应和稳定动脉粥样斑块中的作用。方法 :PPARγ配体 ( 1 5 脱氧前列腺素J2和环格列酮 )干预体外培养的U93 7细胞 ,用四唑盐 (MTT)法检测细胞活力 ,细胞免疫组化法和流式细胞法检测细胞IkBα和MMP1的表达程度。结果 :PPARγ配体在低浓度时不会影响细胞活力 (存活率 >80 % ) ;在 1、3、2 4h,PPARγ激活后均能增加IkBα在细胞内的表达 ,但是随着时间推移 ,这种作用逐渐减弱 ,与佛波醇肉豆蔻酸乙酸酯阳性组相比 ,PPARγ配体组MMP1的表达水平下降 (P <0 .0 1 )。结论 :PPARγ可能通过快速增加IkBα的表达而抑制核因子(NF κB)的活性 ,同时PPARγ可通过或不通过NF κB而抑制MMP1的表达 ,从而发挥抑制炎症和增强斑块稳定作用
AIM: To investigate the effects of peroxisome proliferator-activated receptor (PPAR) γ on the expression of nuclear factor-kinases (IkBα) and matrix metalloproteinase-1 (MMP-1) in human monocytes or macrophages and to explore the role of PPARγ in inhibiting inflammation Responses and Stabilization of Atherosclerotic Plaques. METHODS: U93 7 cells cultured in vitro were treated with PPARγ ligand (1 5 deoxy-prostaglandin J2 and ciglitazone). Cell viability was measured by MTT assay. Cell viability was measured by flow cytometry IkBα and MMP1 expression levels. RESULTS: PPARγ ligands did not affect cell viability at low concentrations (survival> 80%); at 1, 3, 24 h, PPARγ increased IkBα expression in cells, but over time, The effect of PPARγ ligand group decreased compared with that of phorbol myristate acetate positive group (P <0.01). CONCLUSION: PPARγ may inhibit the activity of nuclear factor (NF κB) by rapidly increasing the expression of IkBα. At the same time, PPARγ may inhibit the expression of MMP1 with or without NF κB, thereby inhibiting the inflammation and enhancing the plaque stability