Poster presentation, P83

Official XXIst International Pigment Cell Conference website - 21-24 Sept 2011, Bordeaux - France | updated: September 04 2011

BSP-1 protects melanocytes against oxidative stress-induced cell death and hypopigmentation through MITF upregulation

SPEAKER E. Jung #whois submiter ?
AUTHOR(s) E. Jung, S. Kim, M. Kim, S. Shin, J. Lee, D. Park

BACKGROUND AND OBJECTIVES: The occurrence of oxidative stress has been proposed as a pathogenetic mechanism for melanocyte degeneration in vitiligo. Vitiligo is an acquired condition characterized by depigmented, cutaneous lesions that result from the death of pigment-producing cells, melanocytes. In the epidermis from subjects with active vitiligo, an increased production of H2O2 has been reported and is associated with reduced expression and activity of the antioxidant enzymes. In addition, oxidative stress induces hypopigmentation through downregulation of a microphthalmia (MITF) and MITF dependent-melanogenic enzymes which play important roles not only in the control of differentiation, but also in melanocyte survival. Recently, prostaglandin analogues have been reported to be effective on pigmentation of vitiligo lesions. Additionally, combination of antioxidants and melanogenic inducers was suggested to improve therapeutic efficiency for vitiligo. BSP-1 is kaempferol glycosides and isolated from the Cornus macrophylla Wall. BSP-1 has been reported to have inhibitory activity against 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and quinone reductase 2 (QR2). The effects of BSP-1 on skin have remained unknown. This study was aimed to investigate protective effects of BSP-1 against oxidative stress and its mechanism in human epidermal melanocytes. METHODS: In order to understand the cytoprotective role of BSP-1 on melanocytes, we performed cell viability test using MTT analysis and annexin-V/PI staining assay. Signaling pathways related to cell damage and pigmentation was investigated by measurement of ROS production, lipid peroxidation and expression of antioxidant enzymes and melanogenesis-related genes. Results: We found that BSP-1 significantly inhibited oxidative stress-induced cell death, cellular ROS production and lipid peroxidation in melanocytes. In addition, BSP-1 increased expression of antioxidant enzymes including nrf2, HO-1, catalase and SOD. Furthermore, expression of MITF and its downstream melanogenic enzymes such as tyrosinase and trp-1 was increased by BSP-1. We found that expression of MITF-siRNA significantly reduced protective effect of BSP-1 on oxidative stress-induced cell death. The data support a role of BSP-1 in acute protection of cells to oxidative stress that precedes MITF activation. CONCLUSION: In this report, we present the novel use of BSP-1 for the prevention of oxidative stress and damage in melanocyt



Advertisement from our sponsor:
Astellas Pharma Worldwide

Université de Bordeaux 2 & Conseil Régional Aquitaine