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硒和锌通过抑制氧化损伤以及调节核因子-κB(NF-κB)和核因子E2相关因子2/血红素加氧酶-1(Nrf2/Hmox-1)信号通路的表达,减轻大鼠体内四元金属混合物诱导的神经毒性。

Selenium and zinc alleviate quaternary metal mixture -induced neurotoxicity in rats by inhibiting oxidative damage and modulating the expressions of NF-kB and Nrf2/Hmox-1 pathway.

作者信息

Dike Chinyere, Orish Chinna N, Ezejiofor Anthonet N, Cirovic Ana, Cirovic Aleksandar, Babatunde Bolaji, Sikoki Francis, Orisakwe Orish E

机构信息

African Centre of Excellence for Public Health and Toxicological Research (ACE-PUTOR), University of Port Harcourt, PMB, 5323 Port Harcourt, Choba, Nigeria.

Department of Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, University of Port Harcourt, PMB, 5323 Port Harcourt, Choba, Nigeria.

出版信息

IBRO Neurosci Rep. 2023 Jun 16;15:57-67. doi: 10.1016/j.ibneur.2023.06.003. eCollection 2023 Dec.

DOI:10.1016/j.ibneur.2023.06.003
PMID:37415728
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10320409/
Abstract

BACKGROUND

This study evaluated the potential protective effects of Zn and Se in the cerebellum and cerebral cortex, two fundamentally important brain regions, in albino rats that were exposed to heavy metals mixture (Al, Pb, Hg and Mn).

METHODS

Animals were divided into five groups of seven animals per group with following patterns of exposure, controls group 1 were orally treated with deionized water for 60 days; group 2 was exposed to heavy metal mixture (HMM) with following concentrations (20 mg·kg of Pb body weight; 0.40 mg·kg of Hg; 0.56 mg·kg of Mn; and 35 mg·kg; of Al), while groups 3,4 and 5 were exposed to HMM and orally co-treated with zinc chloride (ZnCl; 0.80 mg/kg), sodium selenite (NaSeO;1.50 mg/kg) and zinc chloride plus sodium selenite (ZnCl + NaSeO) respectively.

RESULTS

Exposure to HMM depressed cellular antioxidant apparatus, induced generation of lipid peroxidation markers (Malondialdehyde and NO), downregulated expression of transcription factors (Nrf2, and NF-kB) and upregulated Caspase 3 levels. HMM potentiated acetylcholinesterase activity and induced moderate histopathological alterations. Nevertheless, Zn, Se and in particular Zn + Se had recovering effects on all mentioned hazardous effects produced by HMM exposure in the cerebral cortex and cerebellum.

CONCLUSIONS

Selenium and zinc exert neuroprotection via Nrf2/NF-kB signaling pathways against quaternary heavy metal mixture-induced impairments in albino Sprague Dawley rats.

摘要

背景

本研究评估了锌和硒对暴露于重金属混合物(铝、铅、汞和锰)的白化大鼠小脑和大脑皮层这两个极其重要的脑区的潜在保护作用。

方法

将动物分为五组,每组七只,采用以下暴露模式:对照组1口服去离子水60天;第2组暴露于重金属混合物(HMM),其浓度如下(每千克体重含20毫克铅;0.40毫克汞;0.56毫克锰;35毫克铝),而第3、4和5组暴露于HMM,并分别口服氯化锌(0.80毫克/千克)、亚硒酸钠(1.50毫克/千克)和氯化锌加亚硒酸钠(ZnCl + NaSeO)进行联合处理。

结果

暴露于HMM会抑制细胞抗氧化机制,诱导脂质过氧化标志物(丙二醛和一氧化氮)的产生,下调转录因子(Nrf2和NF-κB)的表达,并上调半胱天冬酶3水平。HMM增强了乙酰胆碱酯酶活性并诱导了中度组织病理学改变。然而,锌、硒,特别是锌 + 硒对HMM暴露在大脑皮层和小脑中产生的所有上述有害影响具有恢复作用。

结论

硒和锌通过Nrf2/NF-κB信号通路发挥神经保护作用,对抗白化斯普拉格 - 道利大鼠中四元重金属混合物诱导的损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c1f/10320409/a756d4e1e9a0/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c1f/10320409/9beeed32e249/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c1f/10320409/30632b8554a0/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c1f/10320409/b12b0631ee50/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c1f/10320409/098ccbd8e360/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c1f/10320409/f1d6599821b2/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c1f/10320409/a756d4e1e9a0/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c1f/10320409/9beeed32e249/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c1f/10320409/30632b8554a0/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c1f/10320409/b12b0631ee50/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c1f/10320409/098ccbd8e360/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c1f/10320409/f1d6599821b2/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c1f/10320409/a756d4e1e9a0/gr5.jpg

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