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首页> 外文期刊>Food and Nutrition Sciences >Consumption of Oriental Plums Improved the Cognitive Performance and Modulated the Cerebral Neurodegeneration-Related Protein Expressions in Rats with Nicotinamide/Streptozotocin-Induced Diabetes
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Consumption of Oriental Plums Improved the Cognitive Performance and Modulated the Cerebral Neurodegeneration-Related Protein Expressions in Rats with Nicotinamide/Streptozotocin-Induced Diabetes

机译:东方李子的消耗改善了对烟酰胺/链脲佐菌素诱导的糖尿病大鼠的认知性能并调节了大鼠的脑神经变性相关蛋白表达

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To examine the effect of consuming polyphenol-rich Oriental plum (Prunus salicina Lindl) on the cognitive performance and the expressions of cerebral neurodegeneration-related proteins in diabetic rats, Wistar rats were assigned into 4 groups: control (C, n = 14), nicotinamide/streptozotocin-induced DM rats (DM, n = 13), DM rats fed metformin (0.05% w/w in the diet, MT, n = 18), and DM rats fed freeze-dried oriental plum powder (2% w/w in the diet, OP, n = 16) for 2 months. The cognitive performance was evaluated by testing in a Morris water maze. The insulin resistance, serum lipid peroxidation, expressions of pathological proteins of AD, beta-amyloid (Aβ) and phosphorylated tau protein were also measured. Consumption of plums significantly improved the spatial learning ability, reduced the insulin resistance, lipid peroxidation, Aβ and phosphorylated tau protein expressions in the cerebral cortex (all P β deposition in the hippocampus of diabetic rats. In conclusion, polyphenol-rich Oriental plums ameliorated the cognitive decline and reduced the expressions of pathological proteins of AD by possibly reducing hyperglycemia, insulin resistance, and oxidative stress in diabetic rats.
机译:为了检查消耗多酚 - 富苯酚的东方李子(Prunus Salicina Lindl)对糖尿病大鼠中脑神经变性相关蛋白的表达的影响,将Wistar大鼠分配给4组:对照(C,N = 14),烟酰胺/链脲佐菌素诱导的DM大鼠(DM,N = 13),DM大鼠加入二甲双胍(饮食中0.05±W / W,MT,N = 18),DM大鼠加入冷冻干燥的东方李子粉末(2 饮食中的%w / w,op,n = 16)2个月。通过在莫里斯水迷宫中测试来评估认知性能。还测量了胰岛素抵抗,血清脂质过氧化,AD,β-淀粉样蛋白(Aβ)和磷酸化TAU蛋白的病理蛋白表达。李子的消耗显着提高了空间学习能力,降低了脑皮层中的胰岛素抵抗,脂质过氧化,Aβ和磷酸化TAU蛋白表达(糖尿病大鼠海马的所有Pβ沉积。总之,多酚丰富的东方李子改善了通过减少糖尿病大鼠的高血糖,胰岛素抵抗和氧化应激,通过降低糖尿病大鼠的高血糖,胰岛素抵抗和氧化胁迫降低了AD病理蛋白表达。

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