백반증에서 항산화 반응과 자가포식 발현에 대한 면역조직화학적 연구

초록

Background: Oxidative stress is generally accepted as one of the principal pathogenesis of vitiligo, and keratino cyte-melanocyte interactions are also thought to play critical roles. It is well-known that antioxidant response andautophagy protect cells against oxidative damage, but the details and the compensatory relationship between the twomechanisms in the keratinocytes of vitiligo lesions remain unclear. Objective: To evaluate the antioxidant response and autophagy status of patients with vitiligo and to explore theinteractions between these two mechanisms. Methods: Ten patients with clinicopathologically proven vitiligo and 10 normal controls were enrolled in ourDepartment of Dermatology, Soonchunhyang University Hospital, Bucheon, Korea. Tissue samples of vitiligo lesionsin the patient group and normal skin in the control group were immunohistochemically stained for nuclear factorerythroid 2-related factor 2 (Nrf2), Beclin-1, microtubule-associated protein light chain 3 (LC3)-II, and p62. Theimmunopositivity of epidermal keratinocytes was evaluated. Results: Keratinocytes in vitiligo lesions had a significantly lower expression of Nrf2 (p=0.002) than that in thecells of normal controls. The levels of autophagy markers did not differ significantly between the two groups, butdecreases in the Beclin-1 and LC3-II levels, and an increase in the p62 level in the patient group may indicate asmall decrease in autophagy of patients with vitiligo. Conclusion: Decreased antioxidant response and reduced autophagy may trigger melanocyte apoptosis in vitiligolesions.

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