Ajibare Ayodeji Johnson, Akintoye Olabode Oluwadare, Oriowo Oluwatobiloba Adesewa, Asuku Abraham Olufemi, Oriyomi Isaac Adeola, Ayoola Abosede Mary
Neuro-Reproductive and Metabolism Unit, Department of Physiology, Faculty of Basic Medical and Health Sciences, College of Medicine, Lead City University, Ibadan, Oyo State, Nigeria.
Department of Biochemistry, College of Science and Technology, Covenant University, Ota, Ogun State, Nigeria.
Biol Trace Elem Res. 2024 Dec 17. doi: 10.1007/s12011-024-04490-0.
This study investigated the neuromodulatory potential of zinc against acrylamide-induced cognitive impairment. Acrylamide (AA), a toxic substance commonly found in certain foods such as potato, grains and coffee, is known to cause neurological damage and severe cognitive decline. Twenty (20) male Wistar rats were divided into four groups (n = 5) by random selection. All groups except Control (Group 1) which received 1 mL/kg water daily, were induced with an oral dose of 10 mg/kg of Acrylamide. Acrylamide (AA) (Group 2) was left untreated, while Low Zinc (AA + LZN-Group 3) and High zinc (AA + HZN-Group 4) were orally treated respectively with 10 mg/kg and 30 mg/kg of Zinc for 8 weeks. Zinc treatment mitigated the anxiety-like behavior and spatial and non-spatial memory deficit which are all signs of cognitive impairment observed in the AA group. Zinc reverses the significant decrease in superoxide dismutase (SOD) and catalase, significant increase in malondialdehyde (MDA) and interleukin 1β (IL-1β) caused by AA demonstrating its antioxidant and anti-inflammatory properties. Zinc also demonstrated potency in up-regulating brain-derived neurotrophic factor (BDNF) gene expression and down-regulating acetylcholinesterase (AChE) expression. Zinc treatment at both doses significantly increased the number of dentate gyrus cells. This study demonstrates the ability of zinc to mitigate the cognitive impairment secondary to acrylamide exposure.
本研究调查了锌对丙烯酰胺诱导的认知障碍的神经调节潜力。丙烯酰胺（AA）是一种常见于某些食物（如土豆、谷物和咖啡）中的有毒物质，已知会导致神经损伤和严重的认知衰退。通过随机选择将20只雄性Wistar大鼠分为四组（n = 5）。除每天接受1 mL/kg水的对照组（第1组）外，所有组均口服10 mg/kg的丙烯酰胺进行诱导。丙烯酰胺组（第2组）未接受治疗，而低锌组（AA + LZN - 第3组）和高锌组（AA + HZN - 第4组）分别口服10 mg/kg和30 mg/kg的锌，持续8周。锌治疗减轻了焦虑样行为以及空间和非空间记忆缺陷，这些都是在丙烯酰胺组中观察到的认知障碍迹象。锌逆转了由丙烯酰胺引起的超氧化物歧化酶（SOD）和过氧化氢酶的显著降低、丙二醛（MDA）和白细胞介素1β（IL - 1β）的显著增加，证明了其抗氧化和抗炎特性。锌还显示出上调脑源性神经营养因子（BDNF）基因表达和下调乙酰胆碱酯酶（AChE）表达的能力。两种剂量的锌治疗均显著增加了齿状回细胞的数量。本研究证明了锌减轻丙烯酰胺暴露所致认知障碍的能力。
