线粒体功能损伤及机体清除自由基系统功能减弱是诱发胰岛素抵抗和胰岛β细胞功能衰竭，进展为糖尿病的主要机制之一。本项目在前期已纯化并鉴定出4种黑木耳多糖分子结构，发现其降糖途径极有可能与其清除活性氧密切相关，并通过体外胃蠕动模型的建立获得了多糖活性片段的基础上，进一步采用荧光标记获得活性片段的稳定性荧光衍生物，并探明其分子结构信息、口服吸收途径与排除规律及其在胰岛细胞表面识别的靶分子，进而通过其调控胰岛细胞PI3-K mRNA及Bax/Bcl-2的表达，对ATP敏感性钾通道kir6.2 mRNA的表达，对线粒体膜电位、caspase家族等胰岛β细胞凋亡依赖途径的研究以及其改善氧化应激损伤抑制线粒体依赖途径的胰岛细胞凋亡与降糖间相关性的研究阐明其降糖的分子机制，并进一步比对解读其构效关系。本项目对揭示天然多糖防治糖尿病的作用机制以及改善目前糖尿病临床用药存在较大毒副作用的治疗现状意义重大。

Mitochondrial function injury and the free radical scavenging system function abate are the one of the main mechanisms to induce insulin resistance and the pancreatic β-cell apoptosis, and then to make headway type 2 diabetes mellitus. Four sorts of A. auricular polysaccharide were separated and their molecular structures were speculated, and the hypoglycemic pathway of this polysaccharide closely associated with elimination of reactive oxygen species on the basis of the prevenient research, meanwhile, this polysaccharide active fragment through a gastric motility model designed by Leeds university was gained. In the present study, we therefore, plan to investigate their information of molecular structure, the oral absorption pathway and exclusion rule, and the surface recognition of target molecules in islet cell of this polysaccharide, and then to investigate the relevance of the hypoglycemia activity to its antioxidant activity by using rat pancreas tissue as the working model. We shall also evaluate the gene expression of Bcl-2/Bax, the expression of PI3-K in mRNA, the disruption of mitochondrial membrane potential, the repairing of DNA fragmentation, release of cytochrome c from mitochondria to cytosol, activation of caspases and PARP cleavage in the pancreatic tissue of the experimental rats to address the protective mechanism of this polysaccharide. The structure-activity relationship will be explored further. The results of this study, therefore, might shed some light on the reveal the role of natural polysaccharide in the development of type 2 diabetes mellitus.