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

PAPER pubmed Histology and histopathology 2026 Animal study Effect: benefit Evidence: Low

Read original paper → DOI: 10.14670/hh-25-052 PMID: 41742865 Evidence Lab

Abstract

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 using a BL-induced retinal damage model in C57BL/6J mice and using hydrogen peroxide (HO)-induced oxidative stress in 661W photoreceptor cells. Retinal morphology, synaptic integrity, and oxidative stress markers were assessed through histology, immunohistochemistry, and transmission electron microscopy. 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.

AI evidence extraction

At a glance

Study type

Animal study

Effect direction

benefit

Population

C57BL/6J mice; 661W photoreceptor cells (in vitro)

Sample size

—

Exposure

blue light-emitting diode (LED)

Evidence strength

Low

Confidence: 74% · Peer-reviewed: yes

Main findings

In a blue light-induced retinal damage mouse model, Abelmoschus manihot flower extract (AME) pretreatment preserved photoreceptor layer structure, maintained outer segment and synaptic ribbon architecture, and reduced 8-OHdG accumulation. In 661W photoreceptor cells under hydrogen peroxide-induced oxidative stress, AME increased viability, reduced apoptosis, decreased ROS, and increased Nrf2 expression with nuclear translocation.

Outcomes measured

Retinal photoreceptor structural integrity/morphology
Synaptic integrity (synaptic ribbon architecture)
Oxidative stress markers (8-OHdG)
Cell viability (661W cells)
Apoptosis (TUNEL)
Reactive oxygen species (ROS)
Nrf2 expression and nuclear translocation

Limitations

Exposure parameters (e.g., wavelength/intensity/duration) not provided in abstract
Sample size not reported in abstract
Animal and cell models; generalizability to humans not established in abstract

View raw extracted JSON

{
    "study_type": "animal",
    "exposure": {
        "band": null,
        "source": "blue light-emitting diode (LED)",
        "frequency_mhz": null,
        "sar_wkg": null,
        "duration": null
    },
    "population": "C57BL/6J mice; 661W photoreceptor cells (in vitro)",
    "sample_size": null,
    "outcomes": [
        "Retinal photoreceptor structural integrity/morphology",
        "Synaptic integrity (synaptic ribbon architecture)",
        "Oxidative stress markers (8-OHdG)",
        "Cell viability (661W cells)",
        "Apoptosis (TUNEL)",
        "Reactive oxygen species (ROS)",
        "Nrf2 expression and nuclear translocation"
    ],
    "main_findings": "In a blue light-induced retinal damage mouse model, Abelmoschus manihot flower extract (AME) pretreatment preserved photoreceptor layer structure, maintained outer segment and synaptic ribbon architecture, and reduced 8-OHdG accumulation. In 661W photoreceptor cells under hydrogen peroxide-induced oxidative stress, AME increased viability, reduced apoptosis, decreased ROS, and increased Nrf2 expression with nuclear translocation.",
    "effect_direction": "benefit",
    "limitations": [
        "Exposure parameters (e.g., wavelength/intensity/duration) not provided in abstract",
        "Sample size not reported in abstract",
        "Animal and cell models; generalizability to humans not established in abstract"
    ],
    "evidence_strength": "low",
    "confidence": 0.7399999999999999911182158029987476766109466552734375,
    "peer_reviewed_likely": "yes",
    "keywords": [
        "blue light",
        "LED",
        "retina",
        "photoreceptor degeneration",
        "oxidative stress",
        "Abelmoschus manihot",
        "flavonoids",
        "8-OHdG",
        "ROS",
        "Nrf2",
        "C57BL/6J",
        "661W cells"
    ],
    "suggested_hubs": []
}

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AI-extracted fields are generated from the abstract/metadata and may be incomplete or incorrect. This content is for informational purposes only and is not medical advice.

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