Ameliorating effect of Botulinum toxin type A preconditioning on ultraviolet B-induced pigmentation-a novel mechanism associated with inflammation

Ultraviolet B (UVB) is strongly associated with melanin formation, and excess melanin leads to abnormal skin pigmentation. Botulinum toxin type A (BTX-A) can inhibit UVB-induced melanin increase, but the mechanism is not clear.To evaluate the effect of BTX-A on the skin of UVB exposed mice, UVB was applied to the back of each mouse, and UVB was injected with Botox type A as an experimental group. Skin pigmentation, melanin content and tyrosinase (TYR) activity were evaluated. Human epidermal melanocytes and human keratinocytes were co-cultured through in vitro verification. After treatment with BTX-A, cell morphology, growth and density were assessed, caseinase activity and melanin content were assayed. The transcriptome analysis of animal tissues was also performed.BTX-A preconditioning inhibited UVB induced melanin hyperpigmentation. These results indicated that the proliferation of melanocytes increased after UVB irradiation, which promoted melanin secretion, increased TYR activity and aggravated skin pigmentation. Pretreatment with BTX-A can significantly reduce melanin content and reduce skin pigmentation. In terms of mechanism, BTX-A preconditioning inhibits the inflammatory pathway by acting on inflammatory factors including IL-1belt, IL-6 and TNF-alpha, thereby suppressing the proliferation of melanocytes.BTX-A preconditioning can inhibit the inflammatory pathway and reduce UVB-induced melanin hyperpigmentation through IL-1belt, IL-6 and TNF-alpha.