Department of Biochemistry, Faculty of Biological Sciences, University of Nigeria, Nsukka, Nigeria.
Bio-resources Centre Abuja, National Biotechnology Development Agency, Abuja, Nigeria.
Toxicol Mech Methods. 2022 May;32(4):243-258. doi: 10.1080/15376516.2021.1995557. Epub 2021 Nov 15.
Toxic metals such as aluminum accumulation in the brain have been associated with the pathophysiology of several neurodegenerative disorders. leaves contain a vast array of polyphenols, particularly flavonoids, that may play a role in the prevention of toxic and degenerative effects in the brain. This study assessed the neuro-restorative potential of leaves of enriched flavonoid fraction (BPFRF) in aluminum-induced neurotoxicity in rats. Neurotoxicity was induced in male Wistar rats by oral administration of 150 mg/kg body weight of aluminum chloride (AlCl) for 21 days. Rats were grouped into five ( = 6); Control (untreated), Rivastigmine group, AlCl group and BPFRF group (50 and 100 mg/kg b.wt.) for 21 days. Neuronal changes in the hippocampus and cortex were biochemically and histologically evaluated. Expression patterns of acetylcholinesterase (AChE) mRNA were assessed using semi-quantitative reverse-transcription-polymerase chain reaction protocols. Molecular interactions of BPFRF compounds were investigated . The results revealed that oral administration of BPFRF ameliorated oxidative imbalance by augmenting antioxidant systems and decreasing lipid peroxidation caused by AlCl. BPFRF administration also contributed to the down-regulation of AChE mRNA transcripts and improved histological features in the hippocampus and cortex. Molecular docking studies revealed strong molecular interactions between BPFRF compounds, catalase, superoxide dismutase and glutathione peroxidase Overall, these findings suggest the neuroprotective effect of against aluminum-induced neurotoxicity.
有毒金属如铝在大脑中的积累与几种神经退行性疾病的病理生理学有关。 叶含有大量的多酚,特别是类黄酮,它们可能在预防大脑中毒性和退行性作用中发挥作用。本研究评估了富含类黄酮的 叶提取物 (BPFRF) 对铝诱导的大鼠神经毒性的神经修复潜力。通过口服给予雄性 Wistar 大鼠 150mg/kg 体重的氯化铝 (AlCl) 21 天诱导神经毒性。将大鼠分为五组(每组 6 只);对照组(未处理)、利伐斯的明组、AlCl 组和 BPFRF 组(50 和 100mg/kg b.wt.)21 天。使用半定量逆转录聚合酶链反应方案评估海马体和皮质中的神经元变化。使用半定量逆转录聚合酶链反应方案评估乙酰胆碱酯酶 (AChE) mRNA 的表达模式。研究了 BPFRF 化合物的分子相互作用。结果表明,BPFRF 通过增强抗氧化系统和减少 AlCl 引起的脂质过氧化来改善氧化失衡。BPFRF 给药还有助于下调 AChE mRNA 转录本,并改善海马体和皮质的组织学特征。分子对接研究表明,BPFRF 化合物与过氧化氢酶、超氧化物歧化酶和谷胱甘肽过氧化物酶之间存在强烈的分子相互作用。总之,这些发现表明 对铝诱导的神经毒性具有神经保护作用。