Abstract
Antroquinonol was investigated as antioxidant and inhibition of inflammatory responses. Our study was to evaluate its immunosuppressive effect on CD8+ T cells and protective effect on depigmentation. CD8+ T cells were treated with antroquinonol in vitro, and C57BL/6 mice were treated with antroquinonol with or without H2O2 in vivo for 50 consecutive days. We found antroquinonol could inhibit proliferation of CD8+ T cells and suppress the production of cytokines IL-2 and IFN-γ and T cell activation markers CD69 and CD137 in vitro. H2O2 treatment induced depigmentation and reduced hair follicle length, skin thickness, and tyrosinase expression in vivo. Whereas, antroquinonol obviously ameliorated depigmentation of mice skin and resisted the reduction of hair follicle length, skin thickness, and tyrosinase expression induced by H2O2. Antroquinonol decreased CD8+ T cell infiltration in mice skin, inhibited the production of IL-2 and IFN-γ, and decreased the expression of CXCL10 and CXCR3. Summarily, our data shows antroquinonol inhibits CD8+ T cell proliferation in vitro. It also reduces CD8+ T cell infiltration and proinflammatory cytokine secretion and suppresses the thinning of epidermal layer in vivo. Our findings suggest that antroquinonol exerts immunosuppressive effects on CD8+ T cell proliferation and activation to resist depigmentation induced by H2O2.
Highlights
Vitiligo is a common dermatological disorder characterized by the progressive depigmentation caused by a loss of melanocytes in the epidermis
Increased reactive oxygen species (ROS) are thought to be involved in onset of vitiligo, and the infiltration of melanocyte-specific cytotoxic CD8+ T cells into the perilesional margin directly result in melanocyte loss [11, 12]
CD8+ T cells were treated with antroquinonol (0–40 μM) for 48 h, and the results indicated that antroquinonol exhibited inhibition in CD8+ T cell proliferation
Summary
Vitiligo is a common dermatological disorder characterized by the progressive depigmentation caused by a loss of melanocytes in the epidermis. −89 A/T polymorphisms of catalase in vitiligo patients showed significantly increased lipid peroxidation levels [5]. Increased malondialdehyde and decreased catalase were found in vitiligo patient blood [6]. Lymphocyte analysis to peripheral blood of patients with vitiligo showed the total levels of T-cells are normal, but the ratio of CD4+/CD8+ is decreased. Higher number of circulation CD8+ T cells was shown in progressive generalized vitiligo [9]. Increased ROS are thought to be involved in onset of vitiligo, and the infiltration of melanocyte-specific cytotoxic CD8+ T cells into the perilesional margin directly result in melanocyte loss [11, 12]. One study [13] reported that oxidative stress leads to chemokine production and causes CD8+ T
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