The proliferation and migration of vascular smooth muscle cells (VSMCs) are involved in the pathogenesis of intracranial aneurysm (IA) formation and rupture. Interleukin enhancer binding factor 2 (ILF2) is known as the nuclear factor of activated T cells and regulates cell growth. This study was aimed to explore the effects of ILF2 on IA progression. Human brain VSMCs (hBVSMCs) were transfected with pCDNA3.1(+), pCDNA3.1(+)-ILF2, siRNA-negative control, and siRNA-ILF2. The transfection efficiency was then evaluated by determining ILF2 expression. The cell viability and apoptosis were determined using Cell Counting Kit-8 and Annexin V-FITC cell apoptosis assay kit, respectively. Real-time quantification PCR (RT-qPCR) was applied to measure the expression levels of apoptosis-related and inflammation-related genes. Finally, western blot was used to detect the expression level of Fas cell surface death receptor 95 (CD95) and Caspase 8. Overexpression of ILF2 could significantly increase cell viability and decrease cell apoptosis (P < 0.05), while knock-down of ILF2 showed opposite trends for hBVSMCs on cell viability and apoptosis (P < 0.05). RT-qPCR results showed that ILF2 knock-down downregulated the expression levels of BCL2 apoptosis regulator (BCL2), transcriptional regulator Myc-like (c-Myc), and caspase 1 (ICE) whereas upregulated the expression levels of CD95, p21, p53, and interleukin-13 (IL-13). Additionally, the protein expression levels of CD95 and Caspase 8 were significantly decreased after ILF2 overexpression while were significantly increased after ILF2 knock-down (P < 0.05). ILF2 knock-down may inhibit cell viability and promote cell apoptosis of hBVSMCs by regulating the expression levels of apoptosis-related genes and suppressing inflammatory response.

血管平滑肌细胞 (VSMCs) 的增殖和迁移参与了颅内动脉瘤 (IA) 的形成和破裂的发病机制。白细胞介素增强子结合因子 2 ( ILF2 ) 被称为活化 T 细胞的核因子并调节细胞生长。本研究旨在探讨ILF2对 IA 进展的影响。用 pCDNA3.1(+)、pCDNA3.1(+)-ILF2、siRNA 阴性对照和 siRNA-ILF2 转染人脑 VSMC (hBVSMC)。然后通过确定ILF2 来评估转染效率表达。分别使用Cell Counting Kit-8和Annexin V-FITC细胞凋亡测定试剂盒测定细胞活力和凋亡。应用实时定量 PCR (RT-qPCR) 来测量细胞凋亡相关和炎症相关基因的表达水平。最后，采用蛋白质印迹法检测 Fas 细胞表面死亡受体 95 (CD95) 和 Caspase 8 的表达水平。过表达ILF2可显着增加细胞活力并减少细胞凋亡（P  < 0.05），而敲低ILF2显示hBVSMCs 在细胞活力和细胞凋亡方面的趋势相反（P  < 0.05）。RT-qPCR 结果表明ILF2敲低下调 BCL2 凋亡调节因子 ( BCL2 )、转录调节因子 Myc-like ( c-Myc ) 和 caspase 1 ( ICE ) 的表达水平，而上调CD95、p21、p53和白细胞介素-13 ( IL ) 的表达水平-13 )。此外，ILF2过表达后CD95和Caspase 8的蛋白表达水平显着降低，ILF2敲低后显着增加（P  < 0.05）。ILF2 敲低可能通过调节凋亡相关基因的表达水平和抑制炎症反应来抑制 hBVSMCs 的细胞活力并促进细胞凋亡。