衣康酸对百草枯诱导肺泡上皮细胞凋亡的保护作用及机制  

Protective Effect and Mechanism of Itaconate on Paraquat-induced Alveolar Epithelial Cell Apoptosis

作　　者：张敬剑 常晶[1] 周海[1] 郑洪珍 缪翔 莫慧敏 孙洁 郏琴[1] ZHANG Jingjian;CHANG Jing;ZHOU Hai;ZHENG Hongzhen;MIAO Xiang;MO Huimin;SUN Jie;JIA Qin(Department of Respiratory and Critical Care Medicine,Shidong Hospital,Shanghai 200090,China)

机构地区：[1]上海市杨浦区市东医院呼吸与危重症医学科,上海200090

出　　处：《杭州师范大学学报(自然科学版)》2025年第1期64-69,78,共7页Journal of Hangzhou Normal University(Natural Science Edition)

基　　金：上海市杨浦区科学技术委员会、杨浦区卫生健康委员会科研项目(YPQ202104).

摘　　要：为探讨衣康酸在百草枯诱导的肺泡上皮细胞凋亡中的作用及潜在分子机制,采用CCK-8、免疫荧光、RT-qPCR及免疫印迹等技术检测细胞凋亡水平和NF-κB信号通路活性.结果显示,衣康酸显著增强了百草枯抑制的人肺泡上皮细胞株BEAS-2B细胞活力(P<0.05),并抑制了百草枯诱导的Cleaved caspase-3蛋白表达.RT-qPCR结果表明,衣康酸显著降低了促凋亡基因Bax mRNA水平,并提高了抗凋亡基因Bcl-2 mRNA水平(P<0.05).此外,衣康酸减少了NF-κB信号通路中P65蛋白的磷酸化.可见,衣康酸对百草枯诱导的BEAS-2B细胞凋亡具有显著抑制作用,其机制可能与抑制NF-κB信号通路中P65的磷酸化相关.In order to investigate the effect of itaconate acid on the apoptosis of alveolar epithelial cells induced by paraquat and its potential molecular mechanism,the paper used CCK-8,immunofluorescence,RT-qPCR and Western blotting to detect the level of apoptosis and the activity of NF-κB signaling pathway.Itaconate significantly enhanced the viability of human lung epithelial cell line BEAS-2B cells inhibited by paraquat(P<0.05),and significantly inhibited the expression of Cleaved caspase-3 protein induced by paraquat.RT-qPCR results showed that itaconate significantly decreased the mRNA level of pro-apoptotic gene Bax and increased the mRNA level of anti-apoptotic gene[STBX]Bcl-2[STBZ](P<0.05).In addition,itaconate reduced phosphorylation of P65 protein in the NF-κB signaling pathway.In conclusion,itaconate has a significant inhibitory effect on paraquat-induced apoptosis in BEAS-2B cells,and the mechanism may be related to the inhibition of P65 phosphorylation in the NF-κB signaling pathway.

关 键 词：百草枯 衣康酸 肺泡上皮细胞 细胞凋亡 NF-ΚB信号通路 

分 类 号：R563.9[医药卫生—呼吸系统]