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原儿茶酸对镉诱导的 Wistar 大鼠神经毒性和氧化应激中 Na/K-ATP 酶、胆碱能和抗氧化酶活性的影响。

Alterations of Na/K-ATPase, cholinergic and antioxidant enzymes activity by protocatechuic acid in cadmium-induced neurotoxicity and oxidative stress in Wistar rats.

机构信息

Functional Foods and Nutraceuticals Unit, Department of Biochemistry, Federal University of Technology, Akure, Nigeria P.M.B., 704, Akure 340001, Nigeria; Department of Microbiology and Parasitology, Federal University of Santa Maria, Av. Roraima, 97105-900 Santa Maria, RS, Brazil.

Functional Foods and Nutraceuticals Unit, Department of Biochemistry, Federal University of Technology, Akure, Nigeria P.M.B., 704, Akure 340001, Nigeria.

出版信息

Biomed Pharmacother. 2016 Oct;83:559-568. doi: 10.1016/j.biopha.2016.07.017. Epub 2016 Jul 25.

Abstract

BACKGROUND

This study assessed the possible protective mechanisms of protocatechuic acid (PCA) against cadmium (Cd)-induced oxidative stress and neurotoxicity in rats.

METHODS

Male wistar strain rats weighing between 150-160g were purchased and acclimatized for two weeks. The rats were divided into seven groups of seven each; NC group received normal saline, CAD group received 6mg/kg of Cd-solution, CAD+PSG group received Cd-solution and prostigmine (5mg/kg), CAD+PCA-10 and CAD+PCA-20 groups received Cd-solution and PCA (10mg/kg and 20mg/kg) respectively, PCA-10 and PCA-20 groups received 10mg/kg and 20mg/kg PCA each. Animals were administered normal saline, Cd and PCA daily by oral gavage for 21days. After which the animals were sacrificed, the brain excised, homogenized and centrifuged. The activities of enzymes (Na/K-ATPase, cholinesterases, catalase, glutathione peroxidase, superoxide dismutase) and levels of oxidative stress markers (lipid peroxidation and reduced glutathione) linked to neurodegeneration were subsequently assessed.

RESULTS

Significant (p<0.05) alterations in the enzyme activities and levels of oxidative stress markers were observed in CAD group when compared to the NC group. However, the activities of the enzymes were reversed in CAD+PSG and CAD+PCA groups.

CONCLUSIONS

PCA may protect against cadmium-induced neurotoxicity by altering the activities of Na/K-ATPase, acetylcholinesterase, butyrylcholinesterase and endogenous antioxidant enzymes.

摘要

背景

本研究评估了原儿茶酸(PCA)对大鼠镉(Cd)诱导的氧化应激和神经毒性的可能保护机制。

方法

购买雄性 Wistar 品系大鼠,体重在 150-160g 之间,适应环境两周。将大鼠分为七组,每组七只;NC 组给予生理盐水,CAD 组给予 6mg/kg 的 Cd 溶液,CAD+PSG 组给予 Cd 溶液和毒扁豆碱(5mg/kg),CAD+PCA-10 和 CAD+PCA-20 组分别给予 Cd 溶液和 PCA(10mg/kg 和 20mg/kg),PCA-10 和 PCA-20 组给予 PCA 10mg/kg 和 20mg/kg。动物通过口服灌胃每天给予生理盐水、Cd 和 PCA,共 21 天。之后处死动物,取出大脑,匀浆并离心。随后评估与神经退行性变相关的酶(Na/K-ATP 酶、胆碱酯酶、过氧化氢酶、谷胱甘肽过氧化物酶、超氧化物歧化酶)活性和氧化应激标志物(脂质过氧化和还原型谷胱甘肽)水平。

结果

与 NC 组相比,CAD 组的酶活性和氧化应激标志物水平有显著(p<0.05)改变。然而,CAD+PSG 和 CAD+PCA 组的酶活性得到逆转。

结论

PCA 可能通过改变 Na/K-ATP 酶、乙酰胆碱酯酶、丁酰胆碱酯酶和内源性抗氧化酶的活性来预防镉诱导的神经毒性。

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