血小板线粒体功能障碍和损伤（MDD）在糖尿病（DM）血瘀证发病中起重要作用；高糖导致Bcl-xL表达下调诱发MDD引起P选择素（Ps）表达增高；临床研究显示，薯蓣皂苷（Dic）中成药对DM血瘀证疗效明确，但上述机制不详。我们证实，Dic改善MDD并抑制血小板聚集；预研究发现：DM血小板线粒体DNA（mtDNA）含量增高，mtDNA可增加Ps表达，而Dic能降低DM的mtDNA含量及Ps表达。因此，我们推测“高糖抑制Bcl-xL导致MDD，释放mtDNA引发血小板活化；而Dic通过Bcl-xL介导避免MDD，阻断mtDNA外漏”是DM血瘀证发病及Dic防治DM血瘀证的新机制。我们拟用DNA聚合酶-γ基因敲除鼠的DM动物模型、mtDNA缺失血小板的细胞模型，应用激光共聚焦和免疫共沉淀等技术，从整体-细胞-线粒体-分子层次证明我们的假说。此研究有助探明活血化瘀疗效机制，深化糖尿病瘀血阻滞理论。

Mitochondrial dysfunction and damage (MDD) play key roles in blood stasis syndrome of diabetes mellitus(DM).High glucose in DM causes low expression of Bcl-xL,leading to increased expression of p selection (Ps) induced by MDD. Data from clinical research revealed that Diocin(Dic) could reverse blood stasis syndrome of DM, however the underlying mechanism is unknown.Our researh indicated that Dic could alleviate MDD and inhibit platelet aggregation. Meanwhile,we found the high level of mitochondrial DNA (mtDNA) in DM, the increased Ps expression after addition of mtDNA, and the reduced production of mtDNA and Ps expression after Dic treatment.Therefore, we speculate that high glucose causes MDD by supressing Bcl-xL, resulting mtDNA release which trigger platelet activation, while Dio prevents the event induced from high glucose by regulating Bcl-xL to avoid MDD and mtDNA release produced by MDD. It is at the first time proposed that relationship between Bcl-xL and mtDNA release and their roles in blood stasis syndrome of DM, and the interference of Dic and underlying meachanism. Here,we will employ DNA polymerase γ knokout DM mice model，mtDNA knokout platelet model，confocal laser technology，immune coprecipitation techniques to investigate our hypothesis.