Datura metel stramonium exacerbates behavioral deficits, medial prefrontal cortex, and hippocampal neurotoxicity in mice via redox imbalance.

IF 2.7 Q3 MEDICINE, RESEARCH & EXPERIMENTAL Laboratory Animal Research Pub Date : 2023-06-28 DOI:10.1186/s42826-023-00162-7
Vincent Onoriode Igben, Wilson Josiah Iju, Omogbiya Adrian Itivere, John Chukwuma Oyem, Peter Sunday Akpulu, Efe Endurance Ahama
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Abstract

Background: Datura metel (DM) stramonium is a medicinal plant often abused by Nigerians due to its psychostimulatory properties. Hallucinations, confusion, agitation, aggressiveness, anxiety, and restlessness are reported amongst DM users. Earlier studies suggest that DM induces neurotoxicity and affect brain physiology. However, the exact neurological effects of DM extract in the medial prefrontal cortex (mPFC) and hippocampal morphology have not been elucidated. In this study, we evaluated the hypothesis that oral exposure to DM extract exerts a neurotoxic effect by increasing oxidative stress in the mPFC and the hippocampus and induces behavioral deficits in mice.

Results: DM methanolic extract exposure significantly increased MDA and NO levels and reduced SOD, GSH, GPx and CAT activities in mice brains. In addition, our results showed that DM exposure produced cognitive deficits, anxiety, and depressive-like behaviour in mice following oral exposure for 28 days. Moreover, the mPFC and hippocampus showed neurodegenerative features, loss of dendritic and axonal arborization, a dose-dependent decrease in neuronal cell bodies' length, width, area, and perimeter, and a dose-dependent increase in the distance between neuronal cell bodies.

Conclusions: Oral exposure to DM in mice induces behavioural deficits, mPFC and hippocampal neuronal degenerations via redox imbalance in the brain of mice. These observations confirm the neurotoxicity of DM extracts and raises concerns on the safety and potential adverse effects of DM in humans.

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曼陀罗金属流质通过氧化还原不平衡加剧小鼠的行为缺陷、内侧前额叶皮层和海马神经毒性。
背景:曼陀罗金属(DM) stramonium是一种药用植物,由于其精神刺激特性,经常被尼日利亚人滥用。在右美沙芬使用者中有幻觉、混乱、躁动、攻击性、焦虑和不安的报告。早期的研究表明,糖尿病可诱导神经毒性并影响大脑生理。然而,DM提取物对内侧前额叶皮层(mPFC)和海马形态的确切神经学作用尚未阐明。在这项研究中,我们评估了口服DM提取物通过增加小鼠mPFC和海马体的氧化应激而产生神经毒性作用并诱导行为缺陷的假设。结果:DM甲醇提取物显著提高小鼠脑内MDA和NO水平,降低SOD、GSH、GPx和CAT活性。此外,我们的研究结果显示,口服暴露28天后,DM暴露会导致小鼠认知缺陷、焦虑和抑郁样行为。此外,mPFC和海马表现出神经退行性特征,树突和轴突树突的丧失,神经元细胞体的长度、宽度、面积和周长呈剂量依赖性减少,神经元细胞体之间的距离呈剂量依赖性增加。结论:小鼠口服暴露于DM可通过小鼠大脑氧化还原失衡诱导行为缺陷、mPFC和海马神经元变性。这些观察结果证实了DM提取物的神经毒性,并引起了人们对DM在人体中的安全性和潜在副作用的关注。
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来源期刊
CiteScore
4.40
自引率
0.00%
发文量
32
审稿时长
8 weeks
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