期刊论文

Yuan Zhong-Hua

中文

生物化学与生物物理进展

1000-3282

2007

34

10

1055-1064

10.3321/j.issn:1000-3282.2007.10.008

05JJ40039:湖南省自然科学基金 B20042082:湖南省卫生计生委科研项目

本校为第一且通讯机构

以THP-1巨噬细胞为研究对象,观察蛋白激酶C(PKC)激动剂佛波酯(PMA)和抑制剂钙磷酸结合蛋白C(Calphostin C)对胞膜PKC活性、胞膜PKCα及胞浆内过氧化物酶体增殖物激活受体(PPARγ)和adipophilin表达以及细胞内脂质蓄积的影响,初步探讨PKC调控adipophilin表达及脂质蓄积的作用机制.采用PepTag (R) Assay、RT-PCR、蛋白质印迹、油红O染色和高效液相色谱法,观察到100 nmol/L PMA在激活胞膜PKC((0.2514±0.0154)U/ml)的同时可以与氧化低密度脂蛋白(oxLDL)协同增强PKCα、PPARγ和adipophilin表达并使细胞内脂滴的蓄积极大地增强.细胞内胆固醇酯/总胆固醇比值增至(69.8±9.5)%;300 nmol/L Calphostin ...

Several methods, including PepTag (R) Assay, RT-PCR, Western blot, oil red staining and HPLC, were used to explore the role of PKC in lipid-accumulation mediated by adipophilin in THP-1 macrophage treated with PKC activator PMA and inhibitor Calphostin C. 100 nmol/L PMA activated cytomembrane PKC activity ((0.2514 +/- 0.0154) U/ml), also synergistically enhanced the expressions of PKC alpha, PPAR gamma and adipophilin and the lipid-accumulation in the presence of oxLDL. Together with oxLDL, PMA stimulated the ratio of intracellular CE/TC to (69.8 +/- 9.5) %. 300 nmol/L Calphostin C inhibited c...