鉴于AngII/AT1过度激活致内皮功能障碍是缺血再灌注损伤（IRI）的重要原因，而肾素血管紧张素系统(RAS)新通路Ang1-7/Mas能有效对抗其多种生物作用，提示Ang1-7/ AngII平衡在IRI防治中发挥重要作用。我们及他人前期研究显示异丙酚能减轻AngII诱导的内皮细胞凋亡，促进Ang1-7/AngII平衡，推测异丙酚后处理通过干预RAS系统而产生内皮保护作用，但机理尚不明确。本课题拟采用基因转染、信号通路干预等分子生物学手段，在体内、外和信号传导三个层面，观察异丙酚后处理对缺血再灌注后RAS家族、PI3K/Akt/eNOS、内皮功能及心肌损伤等的影响，探讨异丙酚后处理是否通过平衡Ang1-7 / AngII，激活PI3K/Akt/eNOS信号通路而增加NO合成，产生内皮保护作用，揭示异丙酚后处理激发内源性保护效应的新机制，为临床异丙酚有效防治IRI提供理论依据。

?Endothelial cell dysfunction induced by over-activation of AngII/AT1 is an important reason of ischemia-reperfusion injury (IRI). Recent study showed that Ang1-7/Mas pathway, which is a new found RAS pathway, can protect from many pathological effects effectively. This suggests that Ang1-7/Ang II balance may play an important role in IRI. Previous studies found that propofol could reduce angiotensin II-induced endothelial cell apoptosis and promote Ang1-7/AngII. This suggests that propofol IPostC may protect the vascular endothelial cells via interfering the RAS system. However, the mechanism is not clear. This study aims at investigating the role of propofol IPostC on ischemia-reperfusion on in vitro，in vivo and signal transduction levels. By using gene transfection, signaling pathway interfering techniques and so on, we intend to observe the effects of propofol IPostC on the expression of RAS family members, PI3K/Akt/eNOS signaling pathway and myocardial injury. We also intend to find out whether propofol IPostC protects endothelial cells and tissues by balancing Ang1-7/Ang II and activating PI3K/Akt/eNOS signaling pathway, therefore, increasing NO synthesis. This study will reveal a new role and mechanism of propofol IPostC stimulated endogenous protection, therefore, providing a theoretical basis for IRI treatment by propofol in clinical therpeutic.