Activation of p38 MAPK pathway contributes to the melanogenic property of apigenin in B16 cells

Yan Ye, Hui Wang, Jian Hong Chu, Gui Xin Chou, Zhiling YU*

*Corresponding author for this work

Research output: Contribution to journalLetterpeer-review

34 Citations (Scopus)


We investigated the involvement of MAPK pathways in the melanogenic effect of apigenin in B16 cells. Apigenin treatment for 48h dose (5-20μm)-dependently up-regulated protein expression levels of microphthalmia-associated transcription factor (MITF) and melanogenic enzymes including tyrosinase, tyrosinase-related protein-1 (TRP-1) and TRP-2 and enhanced the phosphorylation of p38 MAPK, without affecting the phosphorylation of JNK or ERK MAPK. Treatment with 10μm apigenin time (6-48h)-dependently elevated the protein expressions of p-p38, MITF and melanogenic enzymes. Moreover, PD169316, a selective inhibitor of p38 kinase, suppressed the stimulatory effects of apigenin on tyrosinase activity and melanin synthesis, which were accompanied by decreased MITF protein expression. In conclusion, apigenin increased melanogenesis in B16 cells, at least in part, by activating the p38 MAPK pathway. The novel findings of this study shed light on the molecular mechanisms underlying the melanogenic activity of apigenin and suggest that apigenin/its derivatives may be potentially used for treating hypopigmentation disorders.

Original languageEnglish
Pages (from-to)755-757
Number of pages3
JournalExperimental Dermatology
Issue number9
Publication statusPublished - Sept 2011

Scopus Subject Areas

  • Biochemistry
  • Molecular Biology
  • Dermatology

User-Defined Keywords

  • Apigenin
  • B16 cells
  • MAP kinase
  • Melanogenesis
  • P38


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