International ophthalmology · 2025
Nesfatin-1 alleviates blue-light-emitting diodes induced retinal damage in Sprague-Dawley rats.
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Chekani Azar Saeid, Sabuncuoğlu Nilüfer
Аннотация
PURPOSE: Light-emitting diodes (LEDs) are extensively used across various devices and applications. However, the effects of prolonged or excessive exposure to white and blue LED light on the retina remain inadequately understood.
METHODS: This study investigated the impact of such exposure over 14 weeks on retinal structural and morphological changes and the potential protective effect of nesfatin-1 (N1) administered subcutaneously (0.5 mg/kg body weight) during the final two weeks. Three-week-old Sprague Dawley rats (n = 40) were assigned to six groups: two control groups (C = standard fluorescent lighting; CS = C + sesame oil) and four experimental groups (blue LED, white LED, blue LED + N1, and white LED + N1). Blood and eye samples were collected for biochemical and histopathological analysis at the end of the study.
RESULTS: The blue LED exposure group exhibited significantly elevated serum nesfatin-1 levels (p < 0.001) and reduced concentrations of melatonin and adrenocorticotropic hormone (ACTH; p < 0.05). The retina displayed normal, well-defined structural and morphological features in both control groups, including distinct boundaries and orderly nuclear layer cells between the inner and outer segments. However, slight disorganization of the nuclear layers and a few irregular nuclei were observed in the CS group. Cell loss and damage were more prominent in the LED-exposed groups in both the inner and outer retinal segments and nuclear layers, accompanied by other notable histopathological changes. The inner and outer retinal structures in both white LED groups showed mild disorganization, characterized by irregular nuclei and a noticeable reduction in nuclear layer cells. Retinal damage in both blue LED groups was more pronounced, with marked rod cell loss, disrupted arrangement of the inner and outer plexiform and nuclear layers, and irregular nuclei. Prolonged exposure to blue LED light induced edema in the photoreceptor layers; however, nesfatin-1 administration significantly reduced this inflammation and mitigated other pathological alterations.
CONCLUSION: Biochemical and histological findings indicated that blue LED exposure may disrupt physiological systems by lowering melatonin and ACTH levels, potentially triggering compensatory nesfatin-1 secretion through a rapid feedback mechanism. These results underscore the need for further investigation into the effects of long-term exposure to short-wavelength light on retinal integrity and highlight the possible utility of nesfatin-1 as a biomarker in stress response regulation.
METHODS: This study investigated the impact of such exposure over 14 weeks on retinal structural and morphological changes and the potential protective effect of nesfatin-1 (N1) administered subcutaneously (0.5 mg/kg body weight) during the final two weeks. Three-week-old Sprague Dawley rats (n = 40) were assigned to six groups: two control groups (C = standard fluorescent lighting; CS = C + sesame oil) and four experimental groups (blue LED, white LED, blue LED + N1, and white LED + N1). Blood and eye samples were collected for biochemical and histopathological analysis at the end of the study.
RESULTS: The blue LED exposure group exhibited significantly elevated serum nesfatin-1 levels (p < 0.001) and reduced concentrations of melatonin and adrenocorticotropic hormone (ACTH; p < 0.05). The retina displayed normal, well-defined structural and morphological features in both control groups, including distinct boundaries and orderly nuclear layer cells between the inner and outer segments. However, slight disorganization of the nuclear layers and a few irregular nuclei were observed in the CS group. Cell loss and damage were more prominent in the LED-exposed groups in both the inner and outer retinal segments and nuclear layers, accompanied by other notable histopathological changes. The inner and outer retinal structures in both white LED groups showed mild disorganization, characterized by irregular nuclei and a noticeable reduction in nuclear layer cells. Retinal damage in both blue LED groups was more pronounced, with marked rod cell loss, disrupted arrangement of the inner and outer plexiform and nuclear layers, and irregular nuclei. Prolonged exposure to blue LED light induced edema in the photoreceptor layers; however, nesfatin-1 administration significantly reduced this inflammation and mitigated other pathological alterations.
CONCLUSION: Biochemical and histological findings indicated that blue LED exposure may disrupt physiological systems by lowering melatonin and ACTH levels, potentially triggering compensatory nesfatin-1 secretion through a rapid feedback mechanism. These results underscore the need for further investigation into the effects of long-term exposure to short-wavelength light on retinal integrity and highlight the possible utility of nesfatin-1 as a biomarker in stress response regulation.