molecular mechanisms in the formation and rupture of cerebral aneurysm and impact of drug treatment

Cerebral aneursym的病理学是多功能的。关于如何简化生成、生长和断裂，我们可以在雌激素不良的女性老鼠中建立一个可再生的非线性模型。使用这个模型，我们第一次演示了通过氧化应激和炎症诱导的收缩来减少紧张结合蛋白，以消除内隙，并通过使宏观膜的渗透进入非线性墙。“宏观生长促进炎症中的增加，指导为Vice循环，结果在Cerebral aneurysm的生长和断裂中。要确定某些药物是有可能抑制cerebral neurysms的形成和生长的，我们使用了一类血管紧张素受体I是阻滞剂，磷酸酶4抑制剂， 17·激素替代疗法中的雌二醇和矿皮质激素受体拮抗剂。这些药物是有效的，以防止Cerebral aneurysms的形成和机制根据这些与抗氧化物和反炎症物质有关的药物的作用。在另一手上，他汀类药物产生的多样性效应;有益的和衍生的效应。一个高剂量的沙丁和一个脂性的他汀诱导的断裂。Furthermore，我们发现了一个新的证据，即雌激素缺陷和高盐摄入量的组合与半胱氨酸的形成完全相关。在更进一步的研究中，我们将核实高盐摄入量和高盐肠道之间的关系。

The pathogensis of cerebral aneursysm is multifactorial. To elucidate on how to generate, grow, and rupture, we establish a reproducible aneurysmal model in estrogen deficient female rats. Using this model, we first demonstrated that the reduction of tight junction protein induced by oxidative stress and inflammatory led to the degradation of endothelial gap, thereby facilitating the infiltration of macrophages into the aneurysmal wall. The increase in macrophage promotes inflammation, directed to vice cycle, resulting in the growth and rupture of cerebral aneurysm. To assess whether some drugs are possible to inhibit the formation and growth of cerebral aneurysms, we used an angiotensin typeI receptor a blockade,phosphodiesterase 4 inhibitor, 17・estradiol in hormonal replacement therapy and a mineralcorticoid receptor antagonist.These drugs were effective to prevent the formation of cerebral aneurysms and the mechanism underlying the effects by these drugs associated with anti-oxidative and anti-inflammatory. On the other hand, statins exerted diverse effects; beneficial and deleterious effects. Notably, a high dose satin and a lipophilic statin induced rupture. Furthermore, we found new evidence that the combination of estrogen deficiency and high salt intake is exclusively associated with the formation of cerebral aneurysm. In the further study, we will verify the relationship between high salt intake and cerebral aneurysms.