Medical Research Center, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Department of Zoology, Islamia College Peshawar, Khyber Pakhtunkhwa, Pakistan.
Curr Neuropharmacol. 2024;23(1):116-127. doi: 10.2174/1570159X22999240730154422.
Cadmium chloride (Cd) is a pervasive environmental heavy metal pollutant linked to mitochondrial dysfunction, memory loss, and genetic disorders, particularly in the context of neurodegenerative diseases like Alzheimer's disease (AD).
This study investigated the neurotherapeutic potential of vitamin B6 (Vit. B6) in mitigating Cd-induced oxidative stress and neuroinflammation-mediated synaptic and memory dysfunction. Adult albino mice were divided into four groups: Control (saline-treated), Cd-treated, Cd+Vit. B6- treated, and Vit. B6 alone-treated. Cd and Vit. B6 were administered intraperitoneally, and behavioral tests (Morris Water Maze, Y-Maze) were conducted. Subsequently, western blotting, antioxidant assays, blood glucose, and hyperlipidemia assessments were performed.
Cd-treated mice exhibited impaired cognitive function, while Cd+Vit. B6-treated mice showed significant improvement. Cd-induced neurotoxic effects, including oxidative stress and neuroinflammation, were observed, along with disruptions in synaptic proteins (SYP and PSD95) and activation of p-JNK. Vit. B6 administration mitigated these effects, restoring synaptic and memory deficits. Molecular docking and MD simulation studies confirmed Vit. B6's inhibitory effect on IL-1β, NRF2, and p-JNK proteins.
These results highlight Vit. B6 as a safe therapeutic supplement to mitigate neurodegenerative disorders, emphasizing the importance of assessing nutritional interventions for combating environmental neurotoxicity in the interest of public health.
氯化镉（Cd）是一种普遍存在的环境重金属污染物，与线粒体功能障碍、记忆丧失和遗传紊乱有关，特别是在阿尔茨海默病（AD）等神经退行性疾病的背景下。
本研究调查了维生素 B6（Vit. B6）在减轻 Cd 诱导的氧化应激和神经炎症介导的突触和记忆功能障碍方面的神经治疗潜力。成年白化小鼠分为四组：对照组（生理盐水处理）、Cd 处理组、Cd+Vit. B6 处理组和单独 Vit. B6 处理组。Cd 和 Vit. B6 经腹腔注射给药，并进行行为测试（Morris 水迷宫、Y 迷宫）。随后进行 Western blot、抗氧化测定、血糖和高血脂评估。
Cd 处理组小鼠表现出认知功能受损，而 Cd+Vit. B6 处理组小鼠则显示出显著改善。观察到 Cd 诱导的神经毒性作用，包括氧化应激和神经炎症，以及突触蛋白（SYP 和 PSD95）的破坏和 p-JNK 的激活。Vit. B6 给药减轻了这些影响，恢复了突触和记忆缺陷。分子对接和 MD 模拟研究证实了 Vit. B6 对 IL-1β、NRF2 和 p-JNK 蛋白的抑制作用。
这些结果强调了 Vit. B6 作为一种安全的治疗补充剂，可减轻神经退行性疾病，强调了评估营养干预措施对于对抗环境神经毒性以维护公共健康的重要性。
