The Regulation of Post-inflammatory
Hyperpigmentation by Tranexamic Acid
Abstract
Myoung Shin Kim
Department of Medicine, The Graduate School of the University of Ulsan,
Ulsan, Korea
Background: Although various treatments, such as hydroquinone, vitamin C, glycolic acid,
and Kojic acid have been used for pigmentation disorders, the treatment of postinflammatory
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.
Key words: melanogenesis, postinflammatory hyperpigmentation, tranexamic acid
