【摘要】 目的探讨三磷酸腺苷结合盒运转体 A1(ATP binding cassette transporter A1,ABCA1)在人颈动脉粥样硬化斑块中的表达变化及作用机制。方法收集24例人颈动脉粥样硬化斑块标本和10例肠系膜动脉标本(对照组),采用 RT-PCR 测定 ABCA1 mRNA 和视黄酸 X 受体α(RXRα)mRNA 表达水平,并采用 Western Blot 检测 ABCA1及 RXRα的蛋白表达水平。24例人颈动脉粥样硬化斑块标本按病理分级,比较病理组织为Ⅲ级和Ⅰ级动脉粥样硬化组织间 ABCA1 mRNA、RXRαmRNA 表达水平及蛋白表达水平。结果颈动脉粥样硬化斑块组的 ABCA1 mRNA(0.79±0.04)和RXRα mRNA(0.73±0.04)表达与对照组相比上调,差异有统计学意义(P<0.05);ABCA1 mRNA 与RXRα mRNA 增加水平相关(P<0.05);颈动脉粥样硬化斑块的 ABCA1蛋白表达(0.22±0.03)下调水平与对照组(0.53±0.03)相比差异有统计学意义(P<0.05);Ⅲ级和Ⅰ级动脉硬化斑块 ABCA1mRNA、RXRα mRNA 及蛋白表达水平差异有统计学意义(P<0.05)。结论 ABCA1及 RXRα蛋白表达水平下调可能是进展性动脉粥样硬化损害的关键因素。更多还原

【Abstract】 Objective To investigate the changes of the expressions of ATP-binding cassette transporter A1(ABCA1)and the retinoid X receptor(RXRαin human carotid atherosclerotic plaques and to explore the possible mechanisms by which ABCA1 affects the formation of carotid atherosclerosis(CAS). Methods 24 carotid atherosclerotic plaque and 10 intestinal artery specimens were respectively collected to compared the expression levels of ABCA1 mRNA.RXRαmRNA and those protein,ABCA1 and RXRαgene expressions were determined by reverse transcriptase polymerase chain reaction(RT-PCR)in the specimens,meanwhile the presence of ABCAI and RXRcprotein was assessed by Western blot.Results ABCA1(0.79±0.04)and RXRα(0.73±0.04)gene expression were significantly elevated in carotid atherosclerotic plaques(P<0.05,respectively).The increased levels of ABCA1 mRNA and RXRa mRNA were correlated with each other in carotid atherosclerotic tissue(P<0.05).ABCA1 protein expression (0.22±0.03)was significantly reduced in plaques compared with control tissues(0.53±0.03,P<0.05). Moreover,there were significant differences of levels of ABCAI mRNA and RXRαmRNA and the proteins between plaques of I and III pathological grades.Conclusions Despite the significant upregnlation of ABCA1 mRNA and RXRαmRNA,ABCA1 and RXRαprotein are markedly reduced in advanced carotid atherosclerotic lesions.These findings suggest that the decreased level of ABCA1 and RXRαprotein might play a key role in the pathogenesis of CAS.更多还原