Background: Although various treatments, such as hydroquinone, vitamin C, glycolic acid, and Kojic acid have been used for pigmentation disorders, the treatment of post-inflammatory hyperpigmentation (PIH) is still challenging to dermatologists. In recent years, the curative effect of tranexamic aci...
Background: Although various treatments, such as hydroquinone, vitamin C, glycolic acid, and Kojic acid have been used for pigmentation disorders, the treatment of post-inflammatory hyperpigmentation (PIH) is still challenging to dermatologists. In recent years, the curative effect of tranexamic acid in melasma and UV-induced PIH has been reported in Asian countries. Tranexamic acid is a well-known anti-fibrinolytic drug inhibiting plasmin/plasminogen system, which has been used for preventing blood loss during surgery. In addition to its hemostatic effects, several studies showed that tranexamic acid had inhibitory effect on UV-induced melanogenesis. However, the exact mechanism of the inhibitory effect of tranexamic acid on melanogenesis is not fully understood.
Objectives: To clarify the inhibitory effect of tranexamic acid on PIH, we investigated the effects of tranexamic acid using mouse melanocytes (melan-a cell) and moderately pigmented human melanocytes.
Materials and Methods: Melan-a cell and human melanocytes were cultured with fractional carbon dioxide laser-treated keratinocyte-conditioned media. In cells treated with or without tranexamic acid, we evaluated melanin content and tyrosinase activity. Protein level of tyrosinase, tyrosinase related protein-1 and tyrosinase related protein-2 was evaluated in melan-a cells and signaling pathway molecules involved in melanogenesis were also investigated in human melanocytes. Furthermore, we studied the effect of tranexamic acid in skin explants model.
Results: We found that tranexamic acid-treated melanocytes showed reduced melanin content and tyrosinase activity. Tranexamic acid also decreased the protein level of tyrosinase, tyrosinase related protein-1 and tyrosinase related protein-2. This inhibitory effect on melanogenesis was considered to be involved in several signaling pathways, such as p38 mitogen-activated protein kinase (MAPK) and 90 kDa ribosomal S6 kinase (RSK) pathways. In skin explants model, laser-treated skin showed increased pigmentation on the basal layer of skin compared with control, whereas decreased pigmentation was observed in laser-treated skin with addition of tranexamic acid on day 7.
Conclusion: Our results suggest the tranexamic acid may be effective in laser-induced PIH via regulation of p38 MAPK and RSK signaling pathways.
Background: Although various treatments, such as hydroquinone, vitamin C, glycolic acid, and Kojic acid have been used for pigmentation disorders, the treatment of post-inflammatory hyperpigmentation (PIH) is still challenging to dermatologists. In recent years, the curative effect of tranexamic acid in melasma and UV-induced PIH has been reported in Asian countries. Tranexamic acid is a well-known anti-fibrinolytic drug inhibiting plasmin/plasminogen system, which has been used for preventing blood loss during surgery. In addition to its hemostatic effects, several studies showed that tranexamic acid had inhibitory effect on UV-induced melanogenesis. However, the exact mechanism of the inhibitory effect of tranexamic acid on melanogenesis is not fully understood.
Objectives: To clarify the inhibitory effect of tranexamic acid on PIH, we investigated the effects of tranexamic acid using mouse melanocytes (melan-a cell) and moderately pigmented human melanocytes.
Materials and Methods: Melan-a cell and human melanocytes were cultured with fractional carbon dioxide laser-treated keratinocyte-conditioned media. In cells treated with or without tranexamic acid, we evaluated melanin content and tyrosinase activity. Protein level of tyrosinase, tyrosinase related protein-1 and tyrosinase related protein-2 was evaluated in melan-a cells and signaling pathway molecules involved in melanogenesis were also investigated in human melanocytes. Furthermore, we studied the effect of tranexamic acid in skin explants model.
Results: We found that tranexamic acid-treated melanocytes showed reduced melanin content and tyrosinase activity. Tranexamic acid also decreased the protein level of tyrosinase, tyrosinase related protein-1 and tyrosinase related protein-2. This inhibitory effect on melanogenesis was considered to be involved in several signaling pathways, such as p38 mitogen-activated protein kinase (MAPK) and 90 kDa ribosomal S6 kinase (RSK) pathways. In skin explants model, laser-treated skin showed increased pigmentation on the basal layer of skin compared with control, whereas decreased pigmentation was observed in laser-treated skin with addition of tranexamic acid on day 7.
Conclusion: Our results suggest the tranexamic acid may be effective in laser-induced PIH via regulation of p38 MAPK and RSK signaling pathways.
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