Optimization of Monobenzone-Induced Vitiligo Mouse Model by the Addition of Chronic Stress

Abstract

Vitiligo is a common primary, limited or generalized skin depigmentation disorder. Its pathogenesis is complex, multifactorial and unclear. For this reason, few animal models can simulate the onset of vitiligo, and studies of drug interventions are limited. Studies have found that there may be a pathophysiological connection between mental factors and the development of vitiligo. At present, the construction methods of the vitiligo model mainly include chemical induction and autoimmune induction against melanocytes. Mental factors are not taken into account in existing models. Therefore, in this study, mental inducement was added to the monobenzone (MBEH)-induced vitiligo model. We determined that chronic unpredictable mild stress (CUMS) inhibited the melanogenesis of skin. MBEH inhibited melanin production without affecting the behavioral state of mice, but mice in the MBEH combined with CUMS (MC) group were depressed and demonstrated increased depigmentation of the skin. Further analysis of metabolic differences showed that all three models altered the metabolic profile of the skin. In summary, we successfully constructed a vitiligo mouse model induced by MBEH combined with CUMS, which may be better used in the evaluation and study of vitiligo drugs.

Transcutaneous Auricular Vagus Nerve Stimulation Alleviates Monobenzone-Induced Vitiligo in Mice

“…By affecting immune cell infiltration, taVNS may help to reduce the attack of the immune system on melanocytes, counteracting the development of vitiligo. In addition, previous studies also have reported the successful construction of a chronic stress-induced vitiligo mouse model based on the monobenzone-induced model, in which psychological induction further suppressed melanocyte generation and affected mouse behavior [ 49 , 50 ]. The comprehensive regulation of taVNS may better align with the complex pathophysiological mechanisms of vitiligo, encompassing immune system abnormalities, melanocyte apoptosis, and psychological stress.…”