title: Mechanisms of melanogenesis inhibition by propafenone.
abstract: Melanogenesis is a physiological process that results in the synthesis of melanin pigments, which play a crucial protective role against skin photocarcinogenesis. The present study was conducted to determine the inhibitory effects of propafenone on melanogenesis and to elucidate the molecular events involved in the inhibition of melanogenesis by propafenone. To accomplish this, several experiments were conducted using human epidermal melanocyte cells. The melanin content and cAMP production were evaluated, and western blots for proteins involved in melanogenesis were conducted. The melanin content was significantly inhibited by propafenone in a concentration-dependent manner. To clarify the mechanism of the depigmenting property of propafenone, we examined the involvement of propafenone in cAMP signaling. In the cAMP production assay, the intracellular cAMP level was reduced by propafenone. The level of microphthalmia-associated transcription factor (MITF) protein, the upstream transcription factor of tyrosinase, was also reduced by propafenone. In addition, propafenone inhibited the expression of tyrosinase, TRP-1, and TRP-2. Taken together, the results of our study show that propafenone inhibits melanogenesis by suppressing cAMP production, which is involved in the expression of melanogenesis-related proteins and suggests that propafenone may be an effective inhibitor of hyperpigmentation.
authors.affiliation: Biospectrum Life Science Institute, Seongnam City, Gyunggi Do, Republic of Korea.
authors.forename: Sungran
authors.initials: S
authors.lastname: Huh
authors.forename: Eunsun
authors.initials: E
authors.lastname: Jung
authors.forename: Jienny
authors.initials: J
authors.lastname: Lee
authors.forename: Kyungbaeg
authors.initials: K
authors.lastname: Roh
authors.forename: Ju-Duck
authors.initials: JD
authors.lastname: Kim
authors.forename: Jongsung
authors.initials: J
authors.lastname: Lee
authors.forename: Deokhoon
authors.initials: D
authors.lastname: Park
mesh_terms: D002478:Cells, Cultured; D000242:Cyclic AMP / Q000378:metabolism; D004794:Enzyme Repression; D004817:Epidermis / Q000473:pathology; D006801:Humans; D007370:Interferon Type I / Q000235:genetics / Q000378:metabolism; D019746:Intramolecular Oxidoreductases / Q000235:genetics / Q000378:metabolism; D008543:Melanins / Q000096:biosynthesis*; D008544:Melanocytes / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D051739:Microphthalmia-Associated Transcription Factor / Q000096:biosynthesis / Q000235:genetics; D014442:Monophenol Monooxygenase / Q000235:genetics / Q000378:metabolism*; D011257:Pregnancy Proteins / Q000235:genetics / Q000378:metabolism; D011405:Propafenone / Q000737:chemistry / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects; D012880:Skin Pigmentation / Q000187:drug effects; D026941:Sodium Channel Blockers / Q000737:chemistry / Q000494:pharmacology*
chemical_list: D007370:Interferon Type I; D008543:Melanins; D051739:Microphthalmia-Associated Transcription Factor; D011257:Pregnancy Proteins; D026941:Sodium Channel Blockers; C020947:interferon tau; D011405:Propafenone; D000242:Cyclic AMP; D014442:Monophenol Monooxygenase; D019746:Intramolecular Oxidoreductases; C042501:dopachrome isomerase