HMG-CoA还原酶抑制剂抗肾间质纤维化的作用机制  

The mechanism of HMG-CoA reductase inhibitors against renal interstitial fibrosis

作　　者：敦子倩 王保兴[1] 

机构地区：[1]河北医科大学第三医院肾内科,石家庄050051

出　　处：《中华临床医师杂志（电子版）》2014年第7期115-118,共4页Chinese Journal of Clinicians(Electronic Edition)

摘　　要：HMG-CoA还原酶是胆固醇合成过程中的关键性限速酶,他汀类药物作为HMG-CoA还原酶抑制剂是治疗血脂异常的经典药物,其作用不仅局限于此,多效性还表现在可以改善内皮功能,延缓动脉粥样硬化,抗血栓形成等。导致肾间质纤维的作用机制多种多样,往往表现为炎症细胞、因子等的浸润,肾小管上皮细胞的增殖及凋亡,细胞外基质的沉积,肾小管上皮间充质转分化等。而他汀类药物通过减轻炎症细胞、因子的浸润,抗凋亡、抗氧化应激,减轻细胞外基质沉积等作用延缓肾间质纤维化的进程。现将HMG-CoA还原酶抑制剂抗肾间质纤维化的作用机制作一综述。The 3-hydroxy-3-methylglutaryl coenzyme A（HMG-CoA） reductase inhibitors, commonly called statins, are classic drugs for the treatment of dyslipidemia, which is the key in the process of cholesterol synthesis enzyme as the speed limit. Its effects are not limited to this, add to pleiotropic effects can improve endothelial function, and delay the atherosclerosis, thrombosis, etc. The mechanism of action of renal interstitial fibrosis are diverse, often characterized by inflammatory cells and factors such as infiltration, renal tubular epithelial cell proliferation and apoptosis, extracellular matrix deposition, and endothelial-mesenchymal transition. Whereas statins, have been proposed to be renoprotective, by reducing inflammation cells and factors, resistance to apoptosis and oxidative stress, reduce the effect such as extracellular matrix deposition to delay the process of renal interstitial fibrosis. Now the HMG-CoA reductase inhibitors resistance to the mechanism of action of renal interstitial fibrosis.

关 键 词：羟甲基戊二酰基COA还原酶抑制剂 肾间质纤维化 作用机制 

分 类 号：R363[医药卫生—病理学]