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没食子酸和对香豆酸可减轻大鼠2型糖尿病诱导的神经退行性变。

Gallic acid and p-coumaric acid attenuate type 2 diabetes-induced neurodegeneration in rats.

作者信息

Abdel-Moneim Adel, Yousef Ahmed I, Abd El-Twab Sanaa M, Abdel Reheim Eman S, Ashour Mohamed B

机构信息

Molecular Physiology Division, Zoology Department, Faculty of Science, Beni-Suef University, Beni-Suef, 62511, Egypt.

出版信息

Metab Brain Dis. 2017 Aug;32(4):1279-1286. doi: 10.1007/s11011-017-0039-8. Epub 2017 Jun 2.

Abstract

The brain of diabetics revealed deterioration in many regions, especially the hippocampus. Hence, the present study aimed to evaluate the effects of gallic acid and p-coumaric acid against the hippocampal neurodegeneration in type 2 diabetic rats. Adult male albino rats were randomly allocated into four groups: Group 1 served as control ones and others were induced with diabetes. Group 2 considered as diabetic, and groups 3 and 4 were further orally treated with gallic acid (20 mg/kg b.wt./day) and p-coumaric acid (40 mg/kg b.wt./day) for six weeks. Diabetic rats revealed significant elevation in the levels of serum glucose, blood glycosylated hemoglobin and serum tumor necrosis factor-α, while the level of serum insulin was significantly declined. Furthermore, the brain of diabetic rats showed a marked increase in oxidative stress and a decrease of antioxidant parameters as well as upregulation the protein expression of Bax and downregulation the protein expression of Bcl-2 in the hippocampus. Treatment of diabetic rats with gallic acid and p-coumaric acid significantly ameliorated glucose tolerance, diminished the brain oxidative stress and improved antioxidant status, declined inflammation and inhibited apoptosis in the hippocampus. The overall results suggested that gallic acid and p-coumaric acid may inhibit hippocampal neurodegeneration via their potent antioxidant, anti-inflammatory and anti-apoptotic properties. Therefore, both compounds can be recommended as hopeful adjuvant agents against brain neurodegeneration in diabetics.

摘要

糖尿病患者的大脑在许多区域都出现了退化,尤其是海马体。因此,本研究旨在评估没食子酸和对香豆酸对2型糖尿病大鼠海马体神经退行性变的影响。成年雄性白化大鼠被随机分为四组:第1组作为对照组,其他组诱导糖尿病。第2组被视为糖尿病组,第3组和第4组进一步口服没食子酸(20毫克/千克体重/天)和对香豆酸(40毫克/千克体重/天),持续六周。糖尿病大鼠的血清葡萄糖、糖化血红蛋白和血清肿瘤坏死因子-α水平显著升高,而血清胰岛素水平显著下降。此外,糖尿病大鼠的大脑显示氧化应激显著增加,抗氧化参数降低,海马体中Bax蛋白表达上调,Bcl-2蛋白表达下调。用没食子酸和对香豆酸治疗糖尿病大鼠可显著改善葡萄糖耐量,减轻大脑氧化应激,改善抗氧化状态,减轻炎症并抑制海马体中的细胞凋亡。总体结果表明,没食子酸和对香豆酸可能通过其强大的抗氧化、抗炎和抗凋亡特性抑制海马体神经退行性变。因此,这两种化合物可被推荐为对抗糖尿病患者大脑神经退行性变的有希望的辅助药物。

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