《生命科学》 2014, 26(3): 302-308

胰岛淀粉样多肽诱导β细胞凋亡机制的研究进展

焦　铭，李　笔，陶　敏，黄俊潮^*

(湖北科技学院核技术与化学生物学院，咸宁 437100)

摘　要：2 型糖尿病病变中由人类胰岛淀粉样多肽(hIAPP) 形成的蛋白纤维沉淀被认为是引起β 细胞凋亡的重要原因。目前，hIAPP 诱导β 细胞凋亡的确切机制尚未完全明了，很多研究显示hIAPP 引起的β 细胞膜破裂是hIAPP 产生细胞毒性的主要原因。不仅hIAPP 具有引起膜损伤，从而导致细胞淀粉样改变的细胞毒性机制，一些与错误折叠疾病( 如阿尔兹海默病、帕金森综合征、朊病毒病等) 相关的多肽和蛋白质也具有相同的细胞毒性机理。结合最新研究进展，讨论了hIAPP 与膜的相互作用，阐述了hIAPP 诱导β 细胞凋亡的几种可能机制。

Progress on the mechanism of β-cell apoptosis induced by islet amyloid polypeptide

JIAO Ming， LI Bi， TAO Min， HUANG Jun-Chao^*

(School of Nuclear Technology and Chemistry & Biology， Hubei University of Science and Technology， Xianning 437100， China)

Abstract: The presence of fibrillar protein deposits of human islet amyloid polypeptide (hIAPP) is thought to be related to apoptosis of β-cells in type 2 diabetes mellitus (DM2). The mechanism of hIAPP-induced β-cell apoptosis is not understood. However， there is evidence that hIAPP-induced disruption of β-cell membranes is the cause of hIAPP cytotoxicity. Amyloid cytotoxicity by membrane damage has not only been suggested for hIAPP， but also for peptides and proteins related to other misfolding diseases， including Alzheimer’s disease， Parkinson’s disease， and prion diseases. Here we review the interaction of hIAPP with membranes， and discuss recent progress on the proposed mechanisms of hIAPP-induced membrane damage in relation to β-cell apoptosis in DM2.