Background Androgenetic alopecia (Androgenetic Alopecia) is a genetic disorder caused by dihydrotestosterone (DHT), accompanied by the senescence of androgen-sensitive dermal papilla cells (DPCs) located in the base of hair follicles. DHT causes DPC senescence in Androgenetic Alopecia through mitochondrial dysfunction. However...
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Androgenetic Alopecia mice model was used to study the cyanidins on DHT-induced hair growth deceleration.
Results
Cyanidin 3-
O-arabinoside (C3A) effectively decreased DHT-induced mtROS accumulation in DPCs, and C3A reversed the DHT-induced DPC senescence. Excessive mitochondrial calcium accumulation was blocked by C3A. C3A inhibited p38-mediated voltage-dependent anion channel 1 (VDAC1) expression that contributes to mitochondria-associated ER membrane (MAM) formation and transfer of calcium via VDAC1–IP3R1 interactions. DHT-induced MAM formation resulted in increase of DPC senescence. In Androgenetic Alopecia mice models, C3A restored DHT-induced hair growth deceleration, which activated hair follicle stem cell proliferation.
Conclusions
C3A is a promising natural compound for Androgenetic Alopecia treatments against DHT-induced DPC senescence through reduction of MAM formation and mitochondrial dysfunction.
