Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025
The therapeutic effect of zinc oxide nanoparticles against lipopolysaccharides on the rats' retina.
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Emara Eman M, El-Sayyad Hassan Ih, Mowafy Amr M, El-Ghaweet Heba A
Аннотация
BACKGROUND: Lipopolysaccharide (LPS), a potent endotoxin, triggers oxidative stress and inflammatory cascades that contribute to retinal degeneration and disruption of the gut-retina axis. Zinc oxide nanoparticles (ZnO NPs) have emerged as promising agents owing to their strong antioxidant and anti-inflammatory activities, yet their role in retinal protection remains underexplored.
OBJECTIVE: This study investigated the protective and therapeutic effects of ZnO NPs against LPS-induced retinal injury, with emphasis on their impact on oxidative stress, inflammatory responses, and gut microbiota composition in mother rats and their offspring.
METHODS: Eight males and forty female albino rats were used. Pregnant rats were divided into four groups: control, LPS-exposed, ZnO NP-treated, and combined treatment. ZnO NPs were administered four times (three doses during gestation and one post-delivery), whereas LPS was injected twice during gestation. Retinal tissues were examined histologically and immunohistochemically for markers of oxidative stress, inflammation, and apoptosis (including PCNA, p53, and vimentin), while gut microbiota composition was assessed by 16S rRNA sequencing.
RESULTS: LPS exposure caused marked retinal degeneration, elevated oxidative and inflammatory markers (mTOR, COX-2, Caspase-3, MDA, and NO), and significant gut microbiota dysbiosis. ZnO NPs treatment ameliorated these effects, improving retinal structure, reducing inflammatory and apoptotic markers, restoring dopamine and serotonin levels, and partially normalizing gut microbial composition by decreasing pathogenic Escherichia coli and Enterococcus devriesei.
CONCLUSION: ZnO NPs exert both protective and therapeutic effects against LPS-induced retinal injury in mother rats and their offspring, potentially through modulation of oxidative stress, suppression of inflammatory signaling, and rebalancing of gut microbiota. These findings highlight their promise as a novel therapeutic approach for retinal disorders associated with systemic inflammation.
OBJECTIVE: This study investigated the protective and therapeutic effects of ZnO NPs against LPS-induced retinal injury, with emphasis on their impact on oxidative stress, inflammatory responses, and gut microbiota composition in mother rats and their offspring.
METHODS: Eight males and forty female albino rats were used. Pregnant rats were divided into four groups: control, LPS-exposed, ZnO NP-treated, and combined treatment. ZnO NPs were administered four times (three doses during gestation and one post-delivery), whereas LPS was injected twice during gestation. Retinal tissues were examined histologically and immunohistochemically for markers of oxidative stress, inflammation, and apoptosis (including PCNA, p53, and vimentin), while gut microbiota composition was assessed by 16S rRNA sequencing.
RESULTS: LPS exposure caused marked retinal degeneration, elevated oxidative and inflammatory markers (mTOR, COX-2, Caspase-3, MDA, and NO), and significant gut microbiota dysbiosis. ZnO NPs treatment ameliorated these effects, improving retinal structure, reducing inflammatory and apoptotic markers, restoring dopamine and serotonin levels, and partially normalizing gut microbial composition by decreasing pathogenic Escherichia coli and Enterococcus devriesei.
CONCLUSION: ZnO NPs exert both protective and therapeutic effects against LPS-induced retinal injury in mother rats and their offspring, potentially through modulation of oxidative stress, suppression of inflammatory signaling, and rebalancing of gut microbiota. These findings highlight their promise as a novel therapeutic approach for retinal disorders associated with systemic inflammation.