目的:以人神经胶质瘤U251细胞为研究对象,从p62参与核转录因子κB(NF-κB)信号途径活化角度,探讨柳氮磺吡啶(SAS)抑制NF-κB信号途径和诱导U251细胞发生凋亡的机制。方法:构建p62 siRNA表达载体,MTT法检测细胞生存率,萤光素酶报告基因分析检测NF-κB转录活性,Western blotting法和间接免疫荧光法检测细胞自噬、凋亡。结果:SAS抑制U251 OBJECTIVE: To investigate the inhibitory effect of sulfasalazine (SAS) on NF-κB signaling pathway and the induction of U251 cell proliferation by investigating the role of p62 in the activation of nuclear factor-κB (NF-κB) signaling pathway in human glioma U251 cells Mechanism of apoptosis. Methods: The p62 siRNA expression vector was constructed. The cell viability was detected by MTT assay. The transcription activity of NF-κB was detected by luciferase reporter assay. The autophagy and apoptosis were detected by Western blotting and indirect immunofluorescence. Results: SAS inhibited U251