Umbilical Cord Mesenchymal Stem Cell–Derived Exosomes Preserve Melanocyte Stem Cell Integrity Under Acute Neurogenic Oxidative Stress via Activation of the Nrf2– ARE Pathway in C57BL / 6J Mice

Jingbo Cui; Linxia Duan; Hui Qu; Jing Ning; Zhi Li; Huihua Zhang

doi:10.1111/jocd.70854

April 1, 2026Journal of Cosmetic DermatologyOpen Access

Umbilical Cord Mesenchymal Stem Cell–Derived Exosomes Preserve Melanocyte Stem Cell Integrity Under Acute Neurogenic Oxidative Stress via Activation of the Nrf2– ARE Pathway in C57BL / 6J Mice

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Key Points

This research aims to investigate the protective effects of umbilical cord mesenchymal stem cell-derived exosomes on melanocyte stem cells during oxidative stress.
Utilized huCB-MSC-exosomes to mitigate acute neurogenic oxidative stress.
Evaluated the preservation of melanocyte function in C57BL/6J mice.
Measured activation of the nrf2-ARE pathway as a mechanism of action.
Exosomes significantly reduced signs of oxidative stress in melanocyte stem cells.
Activation of the nrf2-ARE pathway was confirmed, correlating with reduced hair depigmentation.
Melanocyte function was preserved compared to control groups under stress conditions.

Implication

Shows exosomes preserve melanocyte integrity in mice, suggesting a potential treatment for hair depigmentation.

Abstract

HUCB-MSC-Exo alleviates acute neurogenic oxidative stress and preserves melanocyte function by activating the Nrf2-ARE pathway, thereby mitigating stress-induced hair depigmentation in C57BL/6J mice.

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Cite This Study

Cui et al. (2026) studied this question.

synapsesocial.com/papers/69edac794a46254e215b4282 https://doi.org/10.1111/jocd.70854

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Umbilical Cord Mesenchymal Stem Cell–Derived Exosomes Preserve Melanocyte Stem Cell Integrity Under Acute Neurogenic Oxidative Stress via Activation of the Nrf2– ARE Pathway in C57BL / 6J Mice

Key Points

Implication

Abstract

Discussion

Cite This Study

Umbilical Cord Mesenchymal Stem Cell–Derived Exosomes Preserve Melanocyte Stem Cell Integrity Under Acute Neurogenic Oxidative Stress via Activation of the Nrf2– ARE Pathway in C57BL / 6J Mice

Key Points

Implication

Abstract

Discussion

Cite This Study

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