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.

本研究评估了咖啡因（腺苷受体拮抗剂）在青光眼大鼠外侧膝状体以及透明质酸模型的初级视觉皮层中的作用。二十(20)只雄性Long evans大鼠被随机分成四组，每组五只动物。该研究证实，透明质酸（HA）显着诱导眼压从 18 至 35 mmHg 升高，而咖啡因对减轻其减轻视力障碍没有影响；脂质过氧化显着增加，相反，HA 的超氧化物水平降低，咖啡因减弱了这种水平。虽然，咖啡因在维持活神经元细胞数量和显着减少 LGB 和视觉皮层中的肿瘤坏死因子-α 免疫阳性细胞方面显示出改善 HA 诱导的组织病理学变化的能力。这些发现表明，咖啡因在透明质酸暴露后无法降低眼压，但能够通过减轻促氧化介质和消除神经变性来恢复抗氧化失衡。