# Establishment and Validation of a C57BL/6J Mouse Model for Melasma

## TL;DR

Researchers created a reliable mouse model for melasma using UVB light, progesterone, and stress, which shows key features of the human condition and responds to treatment.

## Contribution

A stable and clinically relevant C57BL/6J mouse model for melasma that differentiates from PIH and mimics human responses to treatment.

## Key findings

- The model shows hyperpigmentation, melanin accumulation, and elevated tyrosinase levels similar to human melasma.
- It exhibits systemic oxidative stress and reduced autophagy in lesional skin.
- Tranexamic acid treatment in the model mirrors clinical responses in human patients.

## Abstract

Melasma is a recurrent and treatment‐resistant hyperpigmentation disorder characterized by a complex and multifactorial pathogenesis. However, the lack of a stable and reliable animal model has hindered systematic investigations into its onset and progression. In this study, we established a melasma‐like model in C57BL/6J mice by combining broadband UVB irradiation, intramuscular progesterone administration, and induced emotional stress. The affected skin areas exhibited irregular, brown hyperpigmented patches. Histopathological analysis revealed an accumulation of melanin granules in the epidermis and superficial dermis, elevated levels of tyrosinase (TYR) in both skin and plasma, systemic oxidative stress imbalance, and reduced autophagic activity in the lesional skin. Furthermore, this model displayed distinct differences from a UV‐induced post‐inflammatory hyperpigmentation (PIH) model. Notably, the melasma‐like mice responded to tranexamic acid treatment in a manner that closely resembled clinical outcomes observed in human patients. Collectively, these findings establish a stable, reproducible, and clinically relevant mouse model of melasma, providing a valuable platform for future research into its pathogenesis and treatment.

A melasma‐like mouse model was established in C57BL/6J mice using a combination of UVB irradiation, progesterone administration, and chronic psychological stress. This model replicates key clinical features and biomarker alterations observed in human melasma. Importantly, it is fundamentally distinct from UV‐induced post‐inflammatory hyperpigmentation (PIH) and exhibits a therapeutic response to tranexamic acid treatment.