IGF-1 resist oxidative damage to HaCaT and depigmentation in mice treated with H2O2.
Biochem Biophys Res Commun
; 503(4): 2485-2492, 2018 09 18.
Article
em En
| MEDLINE
| ID: mdl-30208515
ABSTRACT
Vitiligo, an acquired pigmentary disorder of the skin, is characterized by a chronic and progressive loss of melanocyte from the epidermis and follicular reservoir. Growth factor of surrounding cells impacted on melanocytes survival. In this study, lower level of IGF-1 in the lesion was found than that in the donor area of vitiligo patients. IGF-1 improved activation of Nrf2, and inhibited ROS generation and endoplasmic reticulum dilation in HaCaT. C57BL/6 mice were treated with 5% H2O2, and combined with 50⯵g/kg of IGF-1 pre-treatment or not once every day for 50 consecutive days. After 50 days, IGF-1 obviously ameliorated depigmentation of mice skin and reduced hair follicle length, skin thickness and Tyrosinase induced by H2O2. Moreover, IGF-1 significantly suppressed CD8+ T cells infiltration in mice skin, inhibited the production of IL-2 and IFN-γ, and decreased the expression of CXCL10 and CXCR3. Thus, the results indicated that IGF-1 could resist oxidative damage to HaCaT, suppress CD8+ T cells infiltration and pro-inflammatory cytokines secretion, and suppresses the thinning of epidermal layer in vivo. It suggests that IGF-1 inhibits oxidative damage to HaCaT and immunosuppressive effects on CD8+ T cells proliferation and activation to resist depigmentation induced by H2O2. This disclosed its multiple roles in the vitiligo, and shed a light on developing the application potential for IGF-1 in vitiligo.
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Base de dados:
MEDLINE
Assunto principal:
Vitiligo
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Fator de Crescimento Insulin-Like I
Limite:
Animals
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Humans
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article