Protective effects of Abelmoschus manihot flower extracts against blue light-emitting diode light-induced retinal photoreceptor cell damage in vivo and in vitro.

BACKGROUND: Excessive exposure to blue light (BL) from light-emitting diodes (LEDs) induces oxidative stress and photoreceptor degeneration, contributing to retinal damage. Abelmoschus manihot flower extract (AME), rich in flavonoids, possesses antioxidant and anti-inflammatory properties; however, its protective effects on the retina have not been fully elucidated.

METHODS: We investigated the protective effects of AME in vivo using a BL-induced retinal damage model in C57BL/6J mice and in vitro using hydrogen peroxide (H2O2)-induced oxidative stress in 661W photoreceptor cells. Retinal morphology, synaptic integrity, and oxidative stress markers were assessed through histology, immunohistochemistry, and transmission electron microscopy. In vitro analyses included cell viability assays, TUNEL staining, reactive oxygen species (ROS) measurement, and evaluation of nuclear factor erythroid 2-related factor 2 (Nrf2) expression and localization.

RESULTS: AME pretreatment preserved the structural integrity of the photoreceptor layer, maintained outer segment and synaptic ribbon architecture, and reduced 8-hydroxy-2'-deoxyguanosine (8-OHdG) accumulation in BL-exposed retinas. In 661W cells, AME enhanced cell viability, decreased apoptosis, and attenuated ROS production. Furthermore, AME upregulated Nrf2 expression and promoted its nuclear translocation, suggesting activation of the antioxidant response pathway.

CONCLUSIONS: AME exerts protective effects against BL-induced retinal degeneration and oxidative stress-induced photoreceptor apoptosis, potentially through activation of the Nrf2 pathway. These findings highlight the therapeutic potential of AME in preventing or mitigating retinal damage associated with oxidative stress.