Intracranial aneurysm (IA) is a common type of refractory cerebrovascular diseases. Inflammatory responses have been reported to be associated with the pathogenesis of IA. We aimed to study the role of STAT3 on IA formation and inflammatory response. STAT3 expression and clinicopathological factors were analyzed in IA and normal cerebral arteries. mRNA level of STAT3 was detected in normal, unruptured, and ruptured IA tissues by RT-PCR and Western blot. Inflammatory cytokines were examined by ELISA in unruptured, ruptured IA tissues, as well as cells with STAT3 overexpression or knockdown. mRNA of phenotypic modulation-related factors was tested by RT-PCR in STAT3 overexpressing or knockdown VSMCs. STAT3 expression was upregulated in ruptured IA tissues and highly associated with IA diameter and IA type. Inflammatory cytokine secretion was increased in ruptured IA samples and positively correlated with STAT3 expression. STAT3 overexpression led to enhanced expression of SM-α actin, SM-MHC, MMP2, and MMP9, and increased secretion of inflammatory cytokines. Our findings have demonstrated that STAT3 is a key regulator in IA formation by modulating inflammatory cytokine expression.

颅内动脉瘤（IA）是一种常见的难治性脑血管疾病。据报道，炎症反应与 IA 的发病机制有关。我们旨在研究 STAT3 在 IA 形成和炎症反应中的作用。在 IA 和正常脑动脉中分析 STAT3 表达和临床病理因素。通过 RT-PCR 和蛋白质印迹在正常、未破裂和破裂的 IA 组织中检测到 STAT3 的 mRNA 水平。通过 ELISA 在未破裂、破裂的 IA 组织以及具有 STAT3 过表达或敲低的细胞中检查炎性细胞因子。通过 RT-PCR 在 STAT3 过表达或敲低的 VSMC 中测试表型调节相关因子的 mRNA。STAT3 表达在破裂的 IA 组织中上调，并且与 IA 直径和 IA 类型高度相关。在破裂的 IA 样本中炎性细胞因子分泌增加，并与 STAT3 表达呈正相关。STAT3 过表达导致 SM-α 肌动蛋白、SM-MHC、MMP2 和 MMP9 的表达增强，并增加炎性细胞因子的分泌。我们的研究结果表明，STAT3 通过调节炎性细胞因子的表达是 IA 形成的关键调节因子。