精品文档---下载后可任意编辑PI3K-AKT 通路与大鼠蛛网膜下腔出血后基底动脉内皮细胞凋亡的实验讨论的开题报告Title: Experimental Study of the PI3K-AKT Pathway and Endothelial Cell Apoptosis in Basilar Artery after Subarachnoid Hemorrhage in RatsIntroduction:Subarachnoid hemorrhage (SAH) is a devastating type of stroke that can be caused by ruptured aneurysms, resulting in high morbidity and mortality rates. One of the pathological hallmarks of SAH is the occurrence of cerebral vasospasm, which can lead to stroke recurrence and a poorer prognosis. Endothelial cell apoptosis has been identified as an important contributor to cerebral vasospasm after SAH. The PI3K-AKT pathway is known to play a critical role in regulating survival and apoptosis of cells. Therefore, investigating the potential involvement of the PI3K-AKT pathway in endothelial cell apoptosis after SAH may provide insights into the pathogenesis of cerebral vasospasm.Objectives:The aim of this study is to investigate the potential involvement of the PI3K-AKT pathway in endothelial cell apoptosis in basilar artery after SAH in rats.Methods:The study will use a rat SAH model induced by injection of blood into the cisterna magna. The rats will be randomly divided into a control group and an SAH group, with six rats in each group. After the induction of SAH, the rats will be observed for three hours, and then sacrificed. The basilar artery will be harvested and analyzed for endothelial cell apoptosis and protein expression of the PI3K-AKT pathway, including PI3K, AKT, and p-AKT.Expected Results:It is hypothesized that endothelial cell apoptosis will be significantly increased in the SAH group compared to the control group. In addition, the protein expression of the PI3K-精品文档---下载后可任意编辑AKT pathway may be altered in the SAH group, indicating its potential involvement in endothelial cell apoptosis after SAH.Conclusion:The results of this study may increase the understanding of the molecular mechanisms underlying endothelial cell apoptosis after SAH and provide a potential therapeutic target for cerebral vasospasm.
