葡萄籽提取物对丙烯酰胺诱导的小鼠神经毒性抗氧化基因表达和酶活性的上调

Sarah M. Albogami
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引用次数: 1

摘要

gse处理小鼠Gpx1 (P < 0.05)、Prdx3 (P < 0.01)、SOD1 (P < 0.05)和CAT (P < 0.05)表达明显上调。与未处理组相比,丙烯酰胺处理组Gpx1 (P < 0.05)、Prdx3 (P < 0.05)、SOD1 (P < 0.05)和CAT (P < 0.05)显著下调。在丙烯酰胺暴露前或与丙烯酰胺同时使用GSE处理的结果表明,GSE使Gpx1、Prdx3、SOD1和CAT的表达恢复到与对照组相似的水平。丙烯酰胺暴露后,GSE处理后的Gpx1 (P < 0.05)、Prdx3 (P < 0.01)、SOD1 (P < 0.05)和CAT (P < 0.05)与未处理对照组相比,均未表现出对丙烯酰胺的神经保护作用。与未处理的对照组相比,在丙烯酰胺治疗前用葡萄籽治疗的动物,LPO活性没有显著变化,谷胱甘肽水平显著增加。
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Upregulation of Antioxidant Gene Expressions and Enzyme Activity Against Acrylamide-Induced Neurotoxicity in Mice after Grape Seed Extract Treatment
Gpx1 (P < 0.05), Prdx3 (P < 0.01), SOD1 (P < 0.05), and CAT (P < 0.05) significantly upregulated in GSE-treated mice, compared to those in untreated controls. In contrast, Gpx1 (P < 0.05), Prdx3 (P < 0.05), SOD1 (P < 0.05), and CAT (P < 0.05) significantly downregulated in acrylamide-treated mice compared to those in untreated controls. Results of the treatment with GSE before exposure to acrylamide or simultaneously with acrylamide indicated that GSE restored Gpx1, Prdx3, SOD1, and CAT expression to similar levels as those in the control group. GSE treatment after exposure to acrylamide did not exert any neuroprotective effects against acrylamide, as revealed by significant downregulation of Gpx1 (P < 0.05), Prdx3 (P < 0.01), SOD1 (P < 0.05), and CAT (P < 0.05) compared to that in untreated controls. Animals treated with grape seed before acrylamide treatment showed no significant change in LPO activities and a significant increase in GSH levels, compared to those in untreated controls.
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