인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
DBpia AI
AI 에이전트
AI 아이디어
AI 리더
AI 뷰어
Citeasy
크롬 서지관리 다운로드
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
Dry eye disease (DED) is a multifactorial ocular disorder marked by tear film instability, oxidative stress, and inflammation. Although melatonin is known to exert antioxidant and anti-inflammatory effects, its precise role in regulating desiccation-induced stress responses at the ocular surface has not been well defined. In particular, the involvement of the Nrf2 signalling pathway in melatonin-mediated protection against corneal epithelial inflammation under tear film instability remains unexplored. In this study, we evaluated the therapeutic potential of melatonin in a human corneal epithelial cell (HCEC) model mimicking desiccation stress. Melatonin treatment significantly reduced reactive oxygen species (ROS) levels and upregulated antioxidant enzymes, including catalase (CAT) and heme oxygenase-1 (HO-1), via Nrf2 pathway activation. These effects were attenuated by Nrf2 knockdown using siRNA, confirming pathway specificity. Furthermore, melatonin markedly suppressed pro-inflammatory cytokine production, suggesting a dual mechanism of action involving both redox regulation and immune modulation. Our findings provide novel insight into the Nrf2-dependent effects of melatonin on ocular surface protection under desiccation conditions. These results suggest melatonin as a promising candidate for the treatment of DED through simultaneous modulation of oxidative and inflammatory pathways specific to tear film instability.
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
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