Caffeine abrogates oxidative stress imbalance: Its implication on lateral geniculate nucleus and visual cortex following hyaluronic acid exposure

•Hyaluronic acid induces tissue damage which lead to elevated intraocular pressure.•Elevated intraocular pressure cause impairment of visual system.•Administration of caffeine abrogates oxidative stress imbalance.•Caffeine does not reduce elevated intraocular pressure. This study assessed the role o...

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Veröffentlicht in:Journal of chemical neuroanatomy 2021-11, Vol.117, p.101996-101996, Article 101996
Hauptverfasser: Adekeye, Adeshina Oloruntoba, Fafure, Adedamola Adediran, Jeje-Pius, Susan Timileyin, Asuquo, Donald Otoabasi, Sanya, Joseph Olurotimi, Ogundipe, Laofe
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Sprache:eng
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Zusammenfassung:•Hyaluronic acid induces tissue damage which lead to elevated intraocular pressure.•Elevated intraocular pressure cause impairment of visual system.•Administration of caffeine abrogates oxidative stress imbalance.•Caffeine does not reduce elevated intraocular pressure. This study assessed the role of caffeine (adenosine receptor antagonist) in the Lateral geniculate body as well as the primary visual cortex of hyaluronic acid model of glaucomatous rats. Twenty (20) male Long evans rats were randomly divided into four groups with five animals each. This research confirmed that hyaluronic acid (HA) significantly induces elevated intraocular pressure from 18 to 35 mmHg and caffeine had no effect on its reduction to palliate visual impairment; There were a significant increase in the lipid peroxidation and conversely decrease in superoxide level with HA which were attenuated by caffeine. Although, caffeine showed a capability of ameliorating the histopathological changes induced by HA in terms of maintenance of a viable neuronal cell count and significant reduction of tumour necrosis factor-α immune positive cells in the LGB and visual cortex. These findings suggest that caffeine was unable to lower the intraocular pressure after hyaluronic acid exposure but has the ability to restore the antioxidant imbalance via mitigating pro-oxidant mediators and abrogate neurodegeneration.
ISSN:0891-0618
1873-6300
DOI:10.1016/j.jchemneu.2021.101996