Department of Biotechnology, College of Science and Humanities, SRM Institute of Science and Technology, Kattankulathur 603 203, Chennai, Tamil Nadu, India.
Department of Conservative Dentistry and Endodontics, Saveetha Dental College and Hospitals, SIMATS, Chennai 600 077, Tamil Nadu, India.
Neurosci Lett. 2022 Nov 1;790:136889. doi: 10.1016/j.neulet.2022.136889. Epub 2022 Sep 27.
Exogenous toxicants cause oxidative stress and damage to brain cells, resulting in inflammation. Neuroinflammation is important in the pathobiology of various neurological illnesses, including Alzheimer's disease (AD). In this context, Bisphenol A (BPA), a common toxin, causes oxidative damage and has been linked to neurological problems. An O-methylated isoflavone known as Biochanin A (5,7-dihydroxy-4'-methoxy-isoflavone, BCA) is considered to be a phytoestrogen, which is abundant in some legume plants and soy which have preventive effects against cancer, osteoporosis, menopausal symptoms and oxidative stress. However, the mechanism by which BCA protected the prenatal neurological stress are not known. So that, in this study we investigated the BCA neuroprotective effect against BPA-induced neuroinflammation in zebrafish embryo models. For this study, fertilized zebrafish embryos are exposed to BPA (1 µM) with or without BCA. Our finding suggested that BCA co-exposure prevented the depletion of antioxidant defense enzymes by BPA and reduced the production of intracellular ROS production, superoxide anion (O), lipid peroxidation (LPO), lactate dehydrogenase (LDH) and nitric oxide (NO) levels in the head that aided in safeguarding neuronal development. Baseline locomotion was rendered and a total distance was calculated to assess the motor function. Exposure to BCA increased acetylcholinestrase (AChE) and improved motor neuron functions. It also reduced the pro-inflammatory response expression and prevented neuroinflammation. Our study suggests that BCA has a positive role in the attenuation or amelioration of neuronal oxidative damage and locomotory behaviour induced by BPA.
外源性毒物会导致氧化应激和脑细胞损伤，从而引发炎症。神经炎症在各种神经疾病的病理生物学中很重要，包括阿尔茨海默病（AD）。在这种情况下，双酚 A（BPA），一种常见的毒素，会造成氧化损伤，并与神经问题有关。一种被称为大豆苷元 A（5,7-二羟基-4'-甲氧基异黄酮，BCA）的 O-甲基化异黄酮被认为是植物雌激素，它在一些豆类植物和大豆中含量丰富，具有预防癌症、骨质疏松症、更年期症状和氧化应激的作用。然而，BCA 保护产前神经应激的机制尚不清楚。因此，在这项研究中，我们研究了 BCA 对斑马鱼胚胎模型中 BPA 诱导的神经炎症的神经保护作用。在这项研究中，受精的斑马鱼胚胎暴露于 BPA（1µM），同时或不暴露于 BCA。我们的研究结果表明，BCA 共暴露可以防止 BPA 耗尽抗氧化防御酶，并减少细胞内 ROS 产生、超氧阴离子（O）、脂质过氧化（LPO）、乳酸脱氢酶（LDH）和头中的一氧化氮（NO）水平，从而有助于保护神经元发育。进行基础运动并计算总距离，以评估运动功能。暴露于 BCA 会增加乙酰胆碱酯酶（AChE）并改善运动神经元功能。它还减少了促炎反应的表达并预防了神经炎症。我们的研究表明，BCA 在减轻或改善 BPA 诱导的神经元氧化损伤和运动行为方面发挥了积极作用。
