Aneurysmal subarachnoid hemorrhage is caused by intracranial aneurysm (IA) rupture and results in high rates of mortality and morbidity. Factors contributing to IA generation, growth and rupture can involve genetics, injury, hemodynamics, environmental factors, and inflammation, in which inflammatory factors are believed to play central roles in the whole natural history. Inflammatory reactions that contribute to IA development may involve synthesis of many functional proteins and expression of genes induced by changes of blood flow, external stimuli such as smoking, internal balance such as hormonal status changes, and blood pressure. Meanwhile, inflammatory reactions itself can evoke inflammatory cytokines release and aggregation such as MMPs, MCP-1, TNF-α and ZO-1, directly or indirectly promoting aneurysm growth and rupture. However, the details of these inflammatory reactions and their action on inflammatory chemokines are still unknown. Moreover, some agents with the function of anti-inflammation, lipid-lowering, antihypertension or inflammatory factor inhibition may have the potential benefit to reduce the risk of aneurysm development or rupture in a group of population despite the underlying mechanism remains unclear. Consequently, we reviewed the potential inflammatory responses and their mechanisms contributing to aneurysm development and rupture and sought intervention targets that may prevent IA rupture or generation.

颅内动脉瘤（IA）破裂引起动脉瘤性蛛网膜下腔出血，导致高死亡率和高发病率。导致IA发生，生长和破裂的因素可能涉及遗传，损伤，血液动力学，环境因素和炎症，其中炎症因素被认为在整个自然历史中起着核心作用。导致IA发生的炎症反应可能涉及许多功能蛋白的合成和由血流变化，外部刺激（如吸烟），内部平衡（如荷尔蒙状态变化）和血压引起的基因表达。同时，炎症反应本身可以引起炎症细胞因子的释放和聚集，例如MMPs，MCP-1，TNF-α和ZO-1，直接或间接促进动脉瘤的生长和破裂。然而，这些炎症反应的细节及其对炎症趋化因子的作用尚不清楚。此外，尽管尚不清楚其基本机制，但某些具有抗发炎，降血脂，抗高血压或炎性因子抑制功能的药物可能具有降低一组人群动脉瘤发展或破裂风险的潜在益处。因此，我们审查了潜在的炎症反应及其促成动脉瘤形成和破裂的机制，并寻求可预防IA破裂或产生的干预目标。尽管尚不清楚其基本机制，但抗高血压或炎性因子抑制可能具有降低人群中动脉瘤发展或破裂风险的潜在益处。因此，我们审查了潜在的炎症反应及其促成动脉瘤形成和破裂的机制，并寻求可预防IA破裂或产生的干预目标。尽管尚不清楚其基本机制，但抗高血压或炎性因子抑制可能具有降低人群中动脉瘤发展或破裂风险的潜在益处。因此，我们审查了潜在的炎症反应及其促成动脉瘤形成和破裂的机制，并寻求可预防IA破裂或产生的干预目标。