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Chem Biol Interact. 2017 Aug 1;273:107-114. doi: 10.1016/j.cbi.2017.06.005. Epub 2017 Jun 7.

Cannabidiol upregulates melanogenesis through CB1 dependent pathway by activating p38 MAPK and p42/44 MAPK.

Author information

1
Department of Dental Hygiene, College of Health Science, Eulji University, Seongnam City, 131-35 Gyunggi Do, Republic of Korea.
2
Department of Marine Science, Incheon National University, 220-12, Incheon City, Republic of Korea.
3
Department of Genetic Engineering, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon City, 164-19 Gyunggi Do, Republic of Korea.
4
COSMAX R&I Center, COSMAX Inc., Seongnam City, 134-86, Gyunggi Do, Republic of Korea.
5
Department of Bio and Chemical Engineering, Hongik University, 300-16, Sejong City, Republic of Korea. Electronic address: shpark74@hongik.ac.kr.
6
Department of Genetic Engineering, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon City, 164-19 Gyunggi Do, Republic of Korea. Electronic address: bioneer@skku.edu.

Abstract

Melanogenesis plays a critical role in the protection of skin against external stresses such as ultraviolet irradiation and oxidative stressors. This study was aimed to investigate the effects of cannabidiol on melanogenesis and its mechanisms of action in human epidermal melanocytes. We found that cannabidiol increased both melanin content and tyrosinase activity. The mRNA levels of microphthalmia-associated transcription factor (MITF), tyrosinase, tyrosinase-related protein (TRP) 1, and TRP2 were increased following cannabidiol treatment. Likewise, cannabidiol increased the protein levels of MITF, TRP 1, TRP 2, and tyrosinase. Mechanistically, we found that cannabidiol regulated melanogenesis by upregulating MITF through phosphorylation of p38 mitogen-activated protein kinase (MAPK) and p42/44 MAPK, independent of cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling. In addition, the melanogenic effect of cannabidiol was found to be mediated by cannabinoid CB1 receptor, not by CB2 receptor. Taken together, these findings indicate that cannabidiol-induced melanogenesis is cannabinoid CB1 receptor-dependent, and cannabidiol induces melanogenesis through increasing MITF gene expression which is mediated by activation of p38 MAPK and p42/44 MAPK. Our results suggest that cannabidiol might be useful as a protective agent against external stresses.

KEYWORDS:

Cannabidiol; Melanin; TRP 1; Tyrosinase; p38 MAPK; p42/44 MAPK

PMID:
28601556
DOI:
10.1016/j.cbi.2017.06.005
[Indexed for MEDLINE]

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