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Naringin ameliorates motor dysfunction and exerts neuroprotective role against vanadium-induced neurotoxicity

机译:柚皮苷可改善运动功能障碍并发挥对钒诱导的神经毒性的神经保护作用

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摘要

Exposure to vanadium has been known to lead to a progressive neurodegenerative disorder like Parkinson's disease. Naringin is a known flavonoid glycoside that is mostly seen in the flesh of grapefruit and orange and is believed to have protective effects for the treatment of neurodegenerative disorders. This study sought to investigate the role of Naringin in the treatment of vanadium-induced neurotoxicity. Vanadium (10 mg/kg BW) was injected intraperitoneally to induce motor dysfunction, followed by treatment with Naringin (30 mg/kg BW) intraperitoneally for 14 days. Oxidative stress imbalance was monitored by checking Glutathione Peroxidase (GPX) and Catalase levels. Histological and immunohistochemical alterations were observed using RBFOX3 polyclonal antibody to determine neuronal cell distribution and NLRP3 inflammasome antibody as a marker of inflammation. Exposure to vanadium induces neurotoxicity by significantly increasing the Catalase and Glutathione Peroxidase (GPX) levels. Vanadium administration also led to increased inflammatory cells and a significant reduction of the viable neuronal cells in the SNc and CPu. Treatment with Naringin showed a neuroprotective role by dependently restoring the Catalase and Glutathione Peroxidase (GPX) levels, inflammasome activation, and neuronal damage in the SNc and CPu. Naringin demonstrated anti-oxidative, and anti-inflammatory responses by inhibiting oxidative stress, and inflammation and exerts neuroprotective effects by inhibiting apoptosis following vanadium-induced neurotoxicity in adult Wistar rats.
机译:众所周知,接触钒会导致帕金森病等进行性神经退行性疾病。柚皮苷是一种已知的类黄酮糖苷,主要存在于葡萄柚和橙子的果肉中,被认为对治疗神经退行性疾病具有保护作用。本研究旨在探讨柚皮苷在治疗钒诱导的神经毒性中的作用。腹膜内注射钒 (10 mg/kg BW) 以诱导运动功能障碍,然后腹膜内注射柚皮苷 (30 mg/kg BW) 治疗 14 天。通过检查谷胱甘肽过氧化物酶 (GPX) 和过氧化氢酶水平来监测氧化应激失衡。使用 RBFOX3 多克隆抗体确定神经元细胞分布,使用 NLRP3 炎性小体抗体作为炎症标志物,观察组织学和免疫组织化学改变。暴露于钒会显着增加过氧化氢酶和谷胱甘肽过氧化物酶 (GPX) 水平,从而诱导神经毒性。钒给药还导致炎症细胞增加,SNc 和 CPu 中活神经元细胞显著减少。柚皮苷处理通过依赖性地恢复 SNc 和 CPu 中的过氧化氢酶和谷胱甘肽过氧化物酶 (GPX) 水平、炎性小体激活和神经元损伤,显示出神经保护作用。柚皮苷通过抑制氧化应激和炎症反应表现出抗氧化和抗炎反应,并通过抑制成年 Wistar 大鼠钒诱导神经毒性后的细胞凋亡来发挥神经保护作用。

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