颅内动脉瘤破裂导致的蛛网膜下腔出血致死率接近50%，因此探讨颅内动脉瘤的发病机制具有十分重要的临床意义。近年来研究认为脑血管壁平滑肌细胞凋亡及炎性细胞浸润等病理变化可能与颅内动脉瘤的形成有关。MSK1及NLK广泛存在于神经系统且二者具有同源性，均可影响细胞的凋亡及炎症反应，那么研究二者在颅内动脉瘤发生机制中所起的作用可能会开辟一个全新的研究方向。本研究拟采用改良高血压诱导法建立大鼠颅内动脉瘤模型，并取下不同时期动脉瘤标本，分别研究MSK1、NLK之间及其与Caspase-3、Bcl-2、Bax、INOS、IL-l0等重要调控分子的内在联系；然后在细胞水平研究干扰MSK1、NLK的表达后各个指标的改变；最后取动脉瘤患者瘤壁标本在临床水平进一步验证MSK1、NLK与上述凋亡及炎症因子之间关系，从而为颅内动脉瘤的研究提供新思路，为下一步颅内动脉瘤的多靶点药物治疗提供理论基础。

The mortality of subarachnoid hemorrhage(SAH)caused by intracranial aneurysm is nearly 50%, therefore, to explore the pathogenesis of intracranial aneurysm is of great clinical significance. Recent studies suggest that some pathological changes including smooth muscle cell apoptosis and inflammatory cells infiltration may be associated with the formation of intracranial aneurysms. MSK1 and NLK have high expression and certain homology in nervous system, both can influence apoptosis and inflammatory response of the nervous system, so studying the function of MSK and NLK involved in aneurysm formation may open a new research direction.This research adopts the improved blood pressure method to set up intracranial aneurysms model, and removed specimens at different times. We will study the expression of MSK1, NLK, Caspase-3, Bcl-2, Bax, INOS, IL-10 respectively and the inner link between them. Then observe changed expression of these cytokines after the interference of MSK1 and NLK on cell level. Finally further verify the relationship between MSK1, NLK and apoptosis and inflammatory factor in clinical level. This research may supply new targets and theoretical basis for the drug therapy of intracranial aneurysm.