自噬-NLRP3炎症体途径在高血压血管内皮损伤中发挥着重要的作用。我们前期研究发现芪七连胶囊具有抗氧化，抑制NLRP3炎症体下游IL-1β、caspase-1等炎性因子的表达以保护血管，其精确的调控机制尚未明确。由此推测芪七连胶囊可能通过调控自噬-NLRP3炎症体途径活性，抑制NLRP3炎症小体活化，从而抑制血管内皮炎症的发生，保护血管内皮。本研究分别以自发性高血压大鼠及AngII诱导人脐静脉内皮细胞为模型，从分子、细胞、动物三个途径探讨芪七连胶囊干预下，自噬-NLRP3炎症体途径中自噬相关因子Beclin-1、LC3-I、LC3-II、P62、NLRP3炎症体相关因子NLRP3、ASC、caspase-1、IL-1β、IL-18及该途径活化因子ROS、NF-κB表达，以探讨芪七连胶囊调节自噬-NLRP3炎症体途径抗血管内皮损伤效应机制，为其临床防治高血压提供服务。

Autophagy-NLRP3 inflammation pathway plays an important role in injury of vascular endothelial of hypertension. Our previous research have shown that the Qiqilian capsules can be antioxidant, inhibit the expression of inflammatory factors of IL-1, protect vascular injury, but the precise regulation mechanism is not yet clear. Thus, we hypothesis: Qiqilian capsules can activate autophagy and inhibit activation of NLRP3 inflammatory cell by inhibiting activity of autophagy-NLRP3 inflammation pathway. So it can inhibit the occurrence of vascular endothelial inflammation and protect vascular endothelial from injury. Taking SHR and human umbilical vascular endothelial cells for the modle respectively, this project will detect the expression of autophagy related factors Beclin-1、LC3-I 、LC3-II and inflammatory NLRP3 ASC, caspase-1, IL-1, IL-18 from the point of morphology、cell and animal under the interference of Qiqilian capsules. So as we will discuss the Qiqilian capsules regulate the effect and mechanism of autophagy-NLRP3 inflammatory corpuscle pathway against vascular endothelial injury, which will provide scientific basis for the prevention and treatment of hypertension clinically.