医药导报2026，Vol.45Issue(8)：1324-1330,7.DOI:10.3870/j.issn.1004-0781.2026.08.003
雷公藤甲素通过铜死亡信号通路抑制HaCaT细胞的增殖
Inhibitory effect of Triptolide on HaCaT Cell Proliferation via the Cuproptosis Signaling Pathway
摘要
Abstract
Objective To investigate the effect of tripolide(TP)on the proliferation of HaCaT cells,and to identify a novel mechanism underlying the anti-psoriatic activity of TP.Methods HaCaT cells were treated with 20 ng·mL-1 tumor necrosis factor-α(TNF-α)for 24 h before subsequent experiments.The effect of TP on HaCaT cell proliferation was assessed using CCK-8 and EdU assays.Reverse transcription quantitative real-time PCR,cellular copper colorimetry,and an ATP assay kit were used to detect the mRNA levels of interleukin(IL)-1β,IL-6,IL-23A and TNF-α,the level of copper ions,and the ATP content in HaCaT cells,respectively.Western blotting,reactive oxygen species(ROS)detection,and mitochondrial membrane potential assay were employed to evaluate the effects of TP alone or in combination with tetrathiomolybdate(TTM)on the expression of cuproptosis-related proteins,ROS production,and mitochondrial membrane potential in HaCaT cells.Results TP significantly inhibited HaCaT cell proliferation(P<0.05),markedly suppressed the mRNA levels of IL-1β,IL-6,IL-23A,and TNF-α(P<0.05),increased copper ion levels(P<0.01),and decreased ATP content(P<0.05).Moreover,TP significantly downregulated the expression of ferredoxin 1,succinate dehydrogenase complex iron-sulfur subunit B,DNA polymerase delta 1,and dihydrolipoamide S-acetyltransferase(P<0.05),promoted ROS generation,and reduced mitochondrial membrane potential(P<0.05).TTM partially reversed the TP-induced abnormalities in the expression of cuproptosis-related proteins.Conclusion TP could inhibit the excessive proliferation of TNF-α-induced HaCaT cells via cuproptosis-related signaling pathways,thereby exerting its anti-psoriatic effect.关键词
雷公藤甲素/HaCaT细胞/银屑病/铜死亡Key words
Triptolide/HaCaT cells/Psoriasis/Cuproptosis分类
医药卫生引用本文复制引用
徐会敏,罗莎莎,贾路路,谭亲友..雷公藤甲素通过铜死亡信号通路抑制HaCaT细胞的增殖[J].医药导报,2026,45(8):1324-1330,7.基金项目
国家自然科学基金资助项目(82160765) （82160765）
广西研究生教育创新计划项目(YCSW2025494). （YCSW2025494）
