慢性间歇性缺氧（CIH）诱导的血小板－内皮粘附是阻塞性睡眠呼吸暂停低通气综合征（OSAHS）促进血栓形成的关键环节，Vps34介导的自噬通路在血栓形成过程中具有重要作用。本课题组前期研究证实，三七总皂苷（PNS）可减少内皮损伤诱导的血小板粘附。因此，本课题假说如下：PNS可抑制CIH诱导的血小板粘附，作用机理与调控Vps34自噬通路相关。围绕这一假说，本研究拟通过建立CIH大鼠模型、CIH损伤内皮－血小板共孵育模型、血小板缺氧模型，证实PNS抑制CIH诱导血小板粘附的疗效，在此基础上，分别采用Vps34及其上游蛋白Ⅰ型PI3K的特异性抑制剂，探索PNS调控Vps34自噬通路发挥上述作用的分子机制。这对应用活血中药防治OSAHS患者血栓事件具有重要的意义。

Platelet adhesion to endothelium induced by chronic intermittent hypoxia (CIH) is crucial for thrombogenesis initiated by obstructive sleep apnea-hypopnea syndrome (OSAHS), where Vps34-mediated autophagy pathway plays a critical role. We reported that Panax notoginseng Saponins (PNS) could inhibit platelet adhesion induced by endothelial cell (EC) injury. We therefore hypothesize that PNS inhibits platelet adhesion induced by CIH via Vps34 autophagy pathway. To test the hypothesis, we choose CIH rat model, CIH-injured EC-platelet co-culture model and platelet hypoxia model to observe the effect of PNS on platelet adhesion and thereafter to illuminate the underlying mechanisms of PNS based on Vps34-autophagy pathway using Vps34 inhibitor and its upstream regulator classⅠPI3K inhibitor. This will provide a new insight into OSAHS treatment with blood-activating herbs.