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ω-3 脂肪酸对大鼠大脑中镉诱导的神经毒性的可能预防作用。

Possible prophylactic effect of omega-3 fatty acids on cadmium-induced neurotoxicity in rats' brains.

机构信息

Department of Biochemistry, Faculty of Science -Alfaisaliah, King Abdulaziz University, PO Box 50212, Jeddah, 21523, Saudi Arabia.

Department of Biochemistry, Faculty of Science -Alfaisaliah, University of Jeddah, PO Box 50212, Jeddah, 21523, Saudi Arabia.

出版信息

Environ Sci Pollut Res Int. 2019 Oct;26(30):31254-31262. doi: 10.1007/s11356-019-06259-8. Epub 2019 Aug 29.

DOI:10.1007/s11356-019-06259-8
PMID:31468353
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6828832/
Abstract

Cadmium (Cd) has long been noted to induce neurodegenerative disorders. Therefore, this study aimed to assess the toxicological impact of Cd on rat brains and evaluate the possible ameliorative impact of omega-3 fatty acids as a protective agent of nervous system. Rats were divided into four groups: group I supplemented orally with saline; group II intoxicated with CdCl (5 mg/kg b.w. orally), and groups III and VI supplemented with omega-3 (100 mg/kg b.w. orally) simultaneously or before CdCl administration, respectively. Cd intoxication induced biochemical and histopathological disturbances in treated rats. Omega-3 fatty acid considerably improved the Cd-associated biochemical changes, reduced the elevation of lipid peroxidation, and normalized the Cd impact on the levels of superoxide dismutase, catalase, glutathione-S-transferases, 8-hydroxydeoxyguanosine, heatshock protein70, nuclear factor-κB, and interferon-γ as well as of neuronal enzymes such as acetylecholinesterase and monoamine oxidase within the brains of treated rats. Additionally, histological findings supported the results that Cd treatment-induced neurodegenerative changes and that polyunsaturated fatty acids act as antioxidants and neuroprotective agents against Cd toxicity. Co-treatment with omega-3 fatty acid was more beneficial than pretreatment. Thus, omega-3 fatty acid should be included in diet to prevent or suppress neurodegenerative disorders caused by continuous exposure to Cd.

摘要

镉(Cd)长期以来一直被认为会引起神经退行性疾病。因此,本研究旨在评估 Cd 对大鼠大脑的毒理学影响,并评估 ω-3 脂肪酸作为神经系统保护剂的可能改善作用。大鼠分为四组:I 组口服补充生理盐水;II 组口服 CdCl(5mg/kg bw)中毒;III 组和 VI 组分别同时或在 CdCl 给药前口服补充 ω-3(100mg/kg bw)。Cd 中毒导致处理大鼠的生化和组织病理学紊乱。ω-3 脂肪酸显著改善了与 Cd 相关的生化变化,降低了脂质过氧化的升高,并使 Cd 对超氧化物歧化酶、过氧化氢酶、谷胱甘肽-S-转移酶、8-羟基脱氧鸟苷、热休克蛋白 70、核因子-κB 和干扰素-γ水平的影响以及大脑中的神经元酶(如乙酰胆碱酯酶和单胺氧化酶)正常化。此外,组织学发现支持了 Cd 处理引起的神经退行性变化的结果,并且多不饱和脂肪酸作为抗氧化剂和神经保护剂对抗 Cd 毒性。与预处理相比,同时治疗更有益。因此,ω-3 脂肪酸应包含在饮食中,以预防或抑制由于持续暴露于 Cd 引起的神经退行性疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/6828832/987f0942ee47/11356_2019_6259_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/6828832/560ef329221a/11356_2019_6259_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/6828832/f512be2e7ece/11356_2019_6259_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/6828832/1e8d133d08ba/11356_2019_6259_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/6828832/76eac179142e/11356_2019_6259_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/6828832/8587afdf541e/11356_2019_6259_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/6828832/987f0942ee47/11356_2019_6259_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/6828832/560ef329221a/11356_2019_6259_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/6828832/f512be2e7ece/11356_2019_6259_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/6828832/1e8d133d08ba/11356_2019_6259_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/6828832/76eac179142e/11356_2019_6259_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/6828832/8587afdf541e/11356_2019_6259_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ed/6828832/987f0942ee47/11356_2019_6259_Fig6_HTML.jpg

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