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Photodermatol Photoimmunol Photomed ; 37(4): 306-312, 2021 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-33404131

RESUMO

BACKGROUND: Despite exhaustive research, melanocyte disappearance and the evolution of vitiligo remain enigmatic, and although multi-factorial, oxidative stress appears as a major player. The role of cutaneous cholinergic system in vitiligo pathogenesis has also been reported in some studies. OBJECTIVE: To evaluate and correlate the influence of phototherapy on cutaneous cholinergic system and oxidative stress in vitiligo. METHODS: Acetyl choline (ACh), its receptors; nicotinic (nAChR) and muscarinic (mAChR); acetylcholine esterase (AChE) and H2 O2 levels were estimated in de-pigmented and re-pigmented lesions of 30 vitiligo patients before and after NB-UVB phototherapy and in 30 controls. ACh and H2 O2 levels were measured by colorimetry. AChE and acetylcholine receptors expression were measured by quantitative real-time PCR. RESULTS: Mean ACh and H2 O2 levels were significantly higher in vitiligo lesions before NB-UVB (P < .001) whereas AChE enzyme level was significantly lower (P < .001) compared to both re-pigmented and control skin. Additionally, mean mAChR was significantly higher and mean nAChR was significantly lower in vitiligo lesions before NB-UVB versus controls and re-pigmented skin (P < .001). Also, H2 O2 and AChE showed negative correlation whereas ACh and mAChR showed significant positive correlation. Although all the studied parameters showed significant changes after treatment and subsequent re-pigmentation, a significant difference continued to exist between all vitiligo skin and controls. CONCLUSION: Cholinergic system is strongly involved in vitiligo pathogenesis through H2 O2 inhibition of AChE which could be reversed by NB-UVB. Moreover, the strong activation of mAChRs may reflect genetic and/or acquired errors, direct up-regulation by ACh and H2 O2 or both.


Assuntos
Terapia Ultravioleta , Vitiligo , Colinérgicos , Humanos , Estresse Oxidativo , Pele , Resultado do Tratamento
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