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作 者:刘杨[1] 张晓膺[1] 罗光华[2] 郑璐[2] 魏江[2] 徐宁[3]
机构地区:[1]苏州大学附属第三医院心胸外科,江苏常州213003 [2]苏州大学附属第三医院综合实验室,江苏常州213003 [3]瑞典隆德大学医院实验医学研究所临床化学系
出 处:《中华临床医师杂志(电子版)》2010年第12期52-55,共4页Chinese Journal of Clinicians(Electronic Edition)
基 金:国家自然科学基金(30972955)
摘 要:目的研究ATP结合盒转运子A1(ABCA1)是否参与肝X受体(LXR)对载脂蛋白M(apoM)的调节。方法分别以LXR激动剂TO901317(TO)与不同浓度的ABCA1阻滞剂DIDS作用人肝癌细胞株(HepG2),通过real-time PCR法检测对apoMmRNA水平的影响。结果与溶剂对照组相比,TO单独作用组apoM mRNA表达水平降低了35.59%(q=5.340,P<0.05),其降低apoM mR-NA的作用不能被DIDS阻断;而25μmol/L TO与400μmol/L DIDS联合作用组apoM mRNA水平的降低程度达58.79%(q=8.821,P<0.001)。结论在HepG2细胞内,ABCA1影响apoM mRNA的表达,但是不参与LXR降低apoM mRNA水平的效应过程,LXR降低apoM的机制还需进一步探讨。Objective To investigate potential role of ABCA1 on LXR mediated regulation of apoM in HepG2 cells. Methods HepG2 cells were incubated with LXR agonist T0901317 with or without ABCA1 antagonist DIDS at different concentrations, and apoM mRNA levels were determined by the real-time RT-PCR. Results TO901317 at 25 μmol/L could significantly inhibit apoM expression in HepG2 cells ( q = 5. 340, P 〈 0. 05), which was not blocked by addition of ABCAI antogonist. Whereas ABCA1 antagonist itself could also inhibit apoM expression in HepG2 cells. T0901317 and DIDS have additive effects on the inhibition of apoM mRNA expression in HepG2 cells ( q = 8. 821 , P 〈 0. 001 ). Conclusions The present study suggested that hepatic apoM expression is also regulated by ABCA1 and LXR mediated inhibition of apoM expression is not via ABCA1 pathway. The detailed mechanism needs further investigation.
关 键 词:ATP结合匣式转运子 载脂蛋白类 基因表达调控 肝X受体
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