Abstract
INTRODUCTION: Impairment of autophagy may be considered a potential mechanism underlying androgenetic alopecia (AGA). The aim of this study was to assess the therapeutic efficacy of platelet-rich plasma (PRP) in AGA treatment and investigate the role of autophagy in this process. METHODS: The experiment was conducted in two phases. In phase I, an AGA mouse model was established and treated with PRP. Following the treatment period, the therapeutic effects on hair growth were evaluated. The expression levels of autophagy-related genes (LC3 and Beclin-1) were assessed using immunohistochemistry (IHC), Western blot (WB), and quantitative real-time PCR (qPCR). In phase II, based on the first phase, additional experimental groups were introduced: (1) AGA model mice treated with the autophagy activator rapamycin (RAPA) alone and (2) AGA model mice receiving combined treatment with PRP and the autophagy inhibitor 3-methyladenine (3-MA). Hair growth progression, histopathological changes in hair follicles, and the expression of autophagy markers were analyzed to elucidate the role of autophagy in PRP-mediated AGA treatment. RESULTS: Results demonstrated that PRP treatment significantly increased both length and weight of newly grown hair in AGA model mice. The AGA model group exhibited markedly reduced mRNA and protein expression levels of autophagy-related markers (LC3 and Beclin-1) compared to controls. PRP intervention substantially enhanced autophagy levels in treated mice. Notably, therapeutic outcomes achieved with RAPA monotherapy were comparable to those observed with PRP treatment. However, the cohort receiving combined PRP and 3-MA treatment showed significantly diminished hair growth parameters (length and weight) and attenuated expression of autophagy-related genes relative to PRP-treated mice. CONCLUSION: Autophagy levels in the hair follicle cells of AGA model mice are reduced, and impaired autophagy may represent a potential pathogenic mechanism underlying AGA. PRP therapy promotes hair growth and alleviates symptoms in AGA model mice by enhancing autophagy.