Department of Biochemistry, University of KwaZulu-Natal, Durban, South Africa.
Department of Biochemistry, Veritas University, Bwari, Nigeria.
J Food Biochem. 2021 Feb;45(2):e13597. doi: 10.1111/jfbc.13597. Epub 2020 Dec 23.
Natural products-based antioxidants have been well reported for their therapeutic benefits in the treatment and management of neurodegenerative diseases. The neuroprotective effect of ursolic acid (UA) against oxidative injury was investigated in isolated rat brain. Induction of oxidative injury in isolated rat brains with 0.1 mM FeSO led to depleted levels of glutathione, superoxide dismutase, catalase, and ENTPDase activities, with concomitant exacerbation of malondialdehyde and nitric oxide levels, α-chymotrypsin, ATPase, and acetylcholinesterase activities. These levels and activities were significantly reversed following treatment of the brain tissues with UA. Molecular docking studies revealed strong molecular interactions between UA, catalase, and ATPase. Overall, these results indicate the neuroprotective effect of UA against oxidative injury in isolated rat brains as depicted by their ability to mitigate oxidative stress, purinergic, and cholinergic dysfunctions, with concomitant suppression of proteolytic activity. PRACTICAL APPLICATIONS: Neurodegenerative diseases are among the common diseases associated with aging and has been implicated as oxidative mediated. Natural products have received increasing recognition in their use as treatment remedy for various oxidative-mediated diseases including neurodegeneration. These natural products include plant secondary metabolites commonly known as phytochemicals. Ursolic acid is a phytochemical usually present in leafy vegetables and fruits. The present study describes the possible therapeutic mechanism of ursolic acid in the amelioration of complications linked to neurodegeneration in oxidative-mediated brain injury. These findings thus give insights into the use of natural products of plant origin in treating and managing neurodegenerative diseases, which may have little or no side effects.
天然产物抗氧化剂因其在治疗和管理神经退行性疾病方面的治疗益处而得到广泛报道。本研究旨在探讨熊果酸(UA)对氧化损伤的神经保护作用。用 0.1mM FeSO4 诱导离体鼠脑氧化损伤,导致谷胱甘肽、超氧化物歧化酶、过氧化氢酶和 ENTPDase 活性降低,同时丙二醛和一氧化氮水平、α-糜蛋白酶、ATPase 和乙酰胆碱酯酶活性加剧。用 UA 处理脑组织后,这些水平和活性显著逆转。分子对接研究显示 UA 与过氧化氢酶和 ATPase 之间存在强烈的分子相互作用。总的来说,这些结果表明 UA 对离体鼠脑氧化损伤具有神经保护作用,能够减轻氧化应激、嘌呤能和胆碱能功能障碍,并同时抑制蛋白水解活性。实际应用:神经退行性疾病是与衰老相关的常见疾病之一,与氧化有关。天然产物因其作为各种氧化介导疾病(包括神经退行性疾病)的治疗方法而受到越来越多的关注。这些天然产物包括植物次生代谢产物,通常称为植物化学物质。熊果酸是一种植物化学物质,通常存在于绿叶蔬菜和水果中。本研究描述了熊果酸在改善氧化介导的脑损伤中与神经退行性相关并发症的可能治疗机制。这些发现为使用植物来源的天然产物治疗和管理神经退行性疾病提供了思路,这些天然产物可能副作用较小或没有副作用。