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目的:观察过氧化物酶体增殖物激活受体γ(PPARγ)信号转导通路在内脂素调控人单核细胞株(THP-1)源性巨噬细胞ATP结合盒转运蛋白A1(ABCA1)表达中的作用,探讨内脂素诱导泡沫细胞形成的机制和途径。方法:THP-1单核细胞诱导分化为巨噬细胞,随机分组,给予不同浓度和不同作用时间的内脂素进行干预,分别运用油红O染色观察细胞浆脂滴变化,反转录聚合酶链反应(RT-PCR)法和蛋白免疫印迹(Westernblot)法检测各组细胞PPARγ及ABCA1mRNA和蛋白表达,酶荧光学法检测细胞内TC和游离胆固醇(FC)含量,TC与FC之差为胆固醇酯(CE)含量。结果:与对照组比较,内脂素干预组细胞浆脂滴明显增多,细胞内FC和CE含量增加(P<0.05),PPARγ及ABCA1mRNA和蛋白表达降低(P<0.05);相关分析显示,内脂素呈浓度和时间依赖性下调PPARγ及ABCA1mRNA和蛋白的表达。结论:内脂素可能通过PPARγ信号转导通路下调ABCA1表达,减少细胞内FC流出,使细胞内CE合成增加,从而诱导泡沫细胞形成。这可能为内脂素致动脉粥样硬化发病机制的研究提供了一个新的理论依据。
OBJECTIVE: To observe the effect of peroxisome proliferator-activated receptor γ (PPARγ) signal transduction pathway on visfatin-regulated THP-1-derived macrophage ATP binding cassette transporter A1 (ABCA1) Expression in the role of visceral adiponectin-induced foam cell formation mechanism and approach. METHODS: THP-1 monocytes were induced to differentiate into macrophages and randomly divided into groups. Interfered with different concentrations and different time of action of visfatin, the lipid droplets were observed by oil red O staining. The expression of reverse transcription polymerase The expression of PPARγ and ABCA1 mRNA and protein were detected by RT-PCR and Western blotting. The content of TC and free cholesterol (FC) in the cells were detected by enzyme-linked immunosorbent assay. The difference between TC and FC was cholesterol Ester (CE) content. Results: Compared with the control group, the amount of lipid droplets in the visceral adipose tissue group increased significantly (P <0.05) and the expression of PPARγ and ABCA1 mRNA and protein decreased (P <0.05) The lipids down-regulated the expression of PPARγ and ABCA1 mRNA and protein in a concentration- and time-dependent manner. Conclusion: The visfatin may down-regulate the expression of ABCA1 through the PPARγ signal transduction pathway, decrease the intracellular FC efflux, increase the intracellular CE synthesis, and induce the formation of foam cells. This may provide a new theoretical basis for the study of the pathogenesis of visfatin-induced atherosclerosis.