Ginsenoside F2 reduces hair loss by controlling apoptosis through the sterol regulatory element-binding protein cleavage activating protein and transforming growth factor-β pathways in a dihydrotestosterone-induced mouse model.
This study was conducted to test whether ginsenoside F2 can reduce hair loss by influencing sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP) and the transforming growth factor beta (TGF-β) pathway of apoptosis in dihydrotestosterone (DHT)-treated hair cells and in a DHT-induced hair loss model in mice. Results for ginsenoside F2 were compared with finasteride. DHT inhibits proliferation of hair cells and induces androgenetic alopecia and was shown to activate an apoptosis signal pathway both in vitro and in vivo. The cell-based 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showed that the proliferation rates of DHT-treated human hair dermal papilla cells (HHDPCs) and HaCaTs increased by 48% in the ginsenoside F2-treated group and by 12% in the finasteride-treated group. Western blot analysis showed that ginsenoside F2 decreased expression of TGF-β2 related factors involved in hair loss. The present study suggested a hair loss related pathway by changing SCAP related apoptosis pathway, which has been known to control cholesterol metabolism. SCAP, sterol regulatory element-binding protein (SREBP) and caspase-12 expression in the ginsenoside F2-treated group were decreased compared to the DHT and finasteride-treated group. C57BL/6 mice were also prepared by injection with DHT and then treated with ginsenoside F2 or finasteride. Hair growth rate, density, thickness measurements and tissue histotological analysis in these groups suggested that ginsenoside F2 suppressed hair cell apoptosis and premature entry to catagen more effectively than finasteride. Our results indicated that ginsenoside F2 decreased the expression of TGF-β2 and SCAP proteins, which have been suggested to be involved in apoptosis and entry into catagen. This study provides evidence those factors in the SCAP pathway could be targets for hair loss prevention drugs.
Department of Oriental Medicinal Materials & Processing, College of Life Science, Kyung Hee University.
Heon-Sub
HS
Shin
Sang-Yong
SY
Park
Eun-Son
ES
Hwang
Don-Gil
DG
Lee
Gafurjon Turdalievich
GT
Mavlonov
Tae-Hoo
TH
Yi
D000505:Alopecia / Q000139:chemically induced* / Q000188:drug therapy*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053454:Caspase 12 / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects; D013196:Dihydrotestosterone; D004195:Disease Models, Animal; D018120:Finasteride / Q000494:pharmacology / Q000627:therapeutic use; D036145:Ginsenosides / Q000494:pharmacology* / Q000627:therapeutic use; D018859:Hair Follicle / Q000187:drug effects / Q000254:growth & development; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism*; D008565:Membrane Proteins / Q000378:metabolism*; D051379:Mice; D015398:Signal Transduction / Q000187:drug effects; D051779:Sterol Regulatory Element Binding Proteins / Q000187:drug effects / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000187:drug effects* / Q000378:metabolism
D036145:Ginsenosides; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; C102196:SREBP cleavage-activating protein; D051779:Sterol Regulatory Element Binding Proteins; D016212:Transforming Growth Factor beta; C407883:ginsenoside F2; D013196:Dihydrotestosterone; D018120:Finasteride; D053454:Caspase 12