OBJECTIVE: To determine whether EA can rescue slow hair regeneration by regulating dihydrotestosterone (DHT)-induced ferroptosis in AGA mice and clarify the effect of EA on DHT-induced ferroptosis in dermal papilla cells (DPCs).
METHODS: Male C57BL/6 mice were used to establish a DHT-induced AGA mouse model, whereas DPCs were used to establish a DHT-induced cellular model. Thereafter, we investigated the therapeutic mechanism of action of EA via immunofluorescence, western blot analysis, immunohistochemistry, electron microscopy, and molecular docking.
RESULTS: EA stimulated hair regeneration in mice and reversed DHT-induced increases in iron content, lipid peroxidation, and DHT-induced mitochondrial dysfunction by activating the Wnt/β-catenin signaling pathway. Further, β-catenin knockdown suppressed the inhibitory effect of EA on DHT-induced ferroptosis in DPCs.
CONCLUSIONS: EA inhibits DHT-induced ferroptosis and promotes hair regrowth in mice by activating the Wnt/β-catenin signaling pathway. Thus, it has potential for use as a treatment option for AGA.
目的:观察电针是否能通过调节二氢睾酮(DHT)诱导的AGA小鼠的铁凋亡来挽救缓慢的毛发再生,并阐明电针对DHT诱导的毛乳头细胞(DPCs)铁凋亡的影响。
方法:用雄性C57BL/6小鼠建立DHT诱导的AGA小鼠模型,而DPC用于建立DHT诱导的细胞模型。此后,我们通过免疫荧光研究了EA的治疗作用机制,蛋白质印迹分析,免疫组织化学,电子显微镜,和分子对接。
结果:EA刺激小鼠毛发再生,逆转DHT诱导的铁含量增加,脂质过氧化,和DHT通过激活Wnt/β-catenin信号通路诱导线粒体功能障碍。Further,β-catenin敲低抑制EA对DHT诱导的DPC中的铁凋亡的抑制作用。
结论:EA通过激活Wnt/β-catenin信号通路抑制DHT诱导的小鼠铁凋亡并促进毛发再生。因此,它有可能用作AGA的治疗选择。