抗器官纤维化短肽——AcSDKP对心脏纤维化的作用及其研究进展  

Effect and Progress of Antifibrotic Tetrapeptide——N-acetyl-seryl-aspartly-lysyl-proline on Inhibition of Heart Fibrosis

作　　者：李淑钰[1] 于婉莹[1] 杨方[1] 

机构地区：[1]河北联合大学医学实验研究中心,河北省唐山市063000

出　　处：《中国动脉硬化杂志》2012年第11期1041-1044,共4页Chinese Journal of Arteriosclerosis

基　　金：国家自然科学基金项目资助(81072254);河北省自然科学基金项目资助(C2011401024)

摘　　要：N-乙酰基-丝氨酰-天门冬氨酰-赖氨酰-脯氨酸(AcSDKP)是一种具有抗器官纤维化作用的由四个氨基酸构成的短肽。正常生理状态下,存在于人的血浆和淋巴系统内。近年研究发现AcSDKP能够抑制诸多器官如心、肺、肾、肝的纤维化。其中可以抑制器官内的靶细胞(如心脏成纤维细胞、肺成纤维细胞、肾小球系膜细胞和肝星状细胞)的增殖和胶原蛋白的合成或表达,通过信号转导系统的调节抑制靶器官内胶原的沉积,减轻致病因素导致的器官纤维化的程度。N-acetyl-seryl-aspartly-lysyl-proline （AcSDKP） is a kind of anti- fibrosis effects of short peptides, which is normally present in human plasma and circulating mononuclear cells. Recent studies found that AcSDKP was involved in some organ＇ s fibrosis, such as heart, lung, kidney and liver. AcSDKP could inhibit the target cells such as cardiac fibro- blasts, lung fibroblasts, glomerular mesangial cells and hepatic stellate cells proliferation and collagen synthesis and expres- sion. Through a variety of mechanisms including extracellular signal transduction AcSDKP can inhibit a target organ within the collagen deposition and reduce the causative factors leading to organ fibrosis.

关 键 词：N-乙酰基-丝氨酰-天门冬氨酰-赖氨酰-脯氨酸 心脏纤维化 转化生长因子β1 血小板源性生长因子 

分 类 号：R363[医药卫生—病理学]