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蓝莓提取物对镉诱导的大鼠脑神经毒性相关生物标志物改变的保护作用——当前终生人类接触该重金属的大鼠模型研究

The Protective Effect of the Supplementation with an Extract from L. Berries against Cadmium-Induced Changes of Chosen Biomarkers of Neurotoxicity in the Brain-A Study in a Rat Model of Current Lifetime Human Exposure to This Toxic Heavy Metal.

机构信息

Department of Toxicology, Medical University of Bialystok, Adama Mickiewicza 2C Street, 15-222 Bialystok, Poland.

出版信息

Int J Mol Sci. 2024 Oct 10;25(20):10887. doi: 10.3390/ijms252010887.

DOI:10.3390/ijms252010887
PMID:39456671
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11507053/
Abstract

Since even low-level environmental exposure to cadmium (Cd) can lead to numerous unfavourable health outcomes, including damage to the nervous system, it is important to recognize the risk of health damage by this xenobiotic, the mechanisms of its toxic influence, and to find an effective protective strategy. This study aimed to evaluate, in a female Wistar rat model of current human environmental exposure to Cd (1 and 5 mg/kg of diet for 3-24 months), if the low-to-moderate treatment with this element can harm the brain and whether the supplementation with a 0.1% L. (Michx.) Elliott berries (chokeberries) extract (AE) can protect against this effect. The exposure to Cd modified the values of various biomarkers of neurotoxicity, including enzymes (acetylcholinesterase (AChE), sodium-potassium adenosine triphosphatase (Na/K-ATPase), phospholipase A2 (PLA2), and nitric oxide synthase 1 (NOS1)) and non-enzymatic proteins (calmodulin (CAM), nuclear factor erythroid 2-related factor 2 (Nrf2), and Kelch-like ECH-associated protein 1 (KEAP1)) crucial for the functioning of the nervous system, as well as the concentrations of calcium (Ca) and magnesium (Mg) and some metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) in the brain tissue. The co-administration of AE, partially or entirely, protected from most of the Cd-induced changes alleviating its neurotoxic influence. In conclusion, even low-level chronic exposure to Cd may adversely affect the nervous system, whereas the supplementation with berries products during the treatment seems a protective strategy.

摘要

由于即使是低水平的环境镉(Cd)暴露也会导致许多不利的健康后果,包括神经系统损伤,因此认识到这种外源性物质的健康损害风险、其毒性影响的机制以及找到有效的保护策略非常重要。本研究旨在评估在当前人类环境 Cd 暴露(饮食中 1 和 5mg/kg,持续 3-24 个月)的雌性 Wistar 大鼠模型中,这种元素的低至中度治疗是否会损害大脑,以及补充 0.1% L. (Michx.) Elliott 浆果(黑果腺肋花楸)提取物(AE)是否可以预防这种影响。Cd 暴露改变了各种神经毒性生物标志物的数值,包括酶(乙酰胆碱酯酶(AChE)、钠钾三磷酸腺苷酶(Na/K-ATPase)、磷脂酶 A2(PLA2)和一氧化氮合酶 1(NOS1))和非酶蛋白(钙调蛋白(CAM)、核因子红细胞 2 相关因子 2(Nrf2)和 Kelch 样 ECH 相关蛋白 1(KEAP1)),这些都是神经系统正常运作所必需的,以及大脑组织中的钙(Ca)和镁(Mg)以及一些金属蛋白酶(MMPs)及其组织抑制剂(TIMPs)的浓度。AE 的共同给药部分或完全保护免受大多数 Cd 诱导的变化,从而减轻其神经毒性影响。总之,即使是低水平的慢性 Cd 暴露也可能对神经系统造成不利影响,而在治疗期间补充浆果产品似乎是一种保护策略。

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