首页> 美国卫生研究院文献>Nutrients >Neuroprotective Potential of Allium sativum against Monosodium Glutamate-Induced Excitotoxicity: Impact on Short-Term Memory Gliosis and Oxidative Stress
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Neuroprotective Potential of Allium sativum against Monosodium Glutamate-Induced Excitotoxicity: Impact on Short-Term Memory Gliosis and Oxidative Stress

机译:大蒜对谷氨酸钠诱导的兴奋性毒性的神经保护潜力:对短期记忆胶质细胞和氧化应激的影响。

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摘要

This study evaluated the neuroprotective potential of against monosodium glutamate (MSG)-induced neurotoxicity with respect to its impact on short-term memory in rats. Forty male Wistar albino rats were assigned into four groups. The control group received distilled water. The second group was administered powder (200 mg/kg of body weight) orally for 7 successive days, then was left without treatment until the 30th day. The third group was injected intraperitoneally with MSG (4 g/kg of body weight) for 7 successive days, then left without treatment until the 30th day. The fourth group was injected with MSG in the same manner as the third group and was treated with powder in the same manner as the second group, simultaneously. Phytochemical analysis of powder identified the presence of diallyl disulphide, carvone, diallyl trisulfide, and allyl tetrasulfide. MSG-induced excitotoxicity and cognitive deficit were represented by decreased distance moved and taking a long time to start moving from the center in the open field, as well as lack of curiosity in investigating the novel object and novel arm. Moreover, MSG altered hippocampus structure and increased MDA concentration and protein expression of glial fibrillary acidic protein (GFAP), calretinin, and caspase-3, whereas it decreased superoxide dismutase (SOD) activity and protein expression of Ki-67 in brain tissue. However, powder prevented MSG-induced neurotoxicity and improved short-term memory through enhancing antioxidant activity and reducing lipid peroxidation. In addition, it decreased protein expression of GFAP, calretinin, and caspase-3 and increased protein expression of Ki-67 in brain tissues and retained brain tissue architecture. This study indicated that powder ameliorated MSG-induced neurotoxicity through preventing oxidative stress-induced gliosis and apoptosis of brain tissue in rats.
机译:这项研究评估了抗谷氨酸钠(MSG)诱导的神经毒性对大鼠短期记忆的神经保护潜力。将40只雄性Wistar白化病大鼠分成四组。对照组接受蒸馏水。第二组连续7天口服粉剂(200 mg / kg体重),然后不治疗直到第30天。第三组连续7天腹膜内注射味精(4 g / kg体重),然后不治疗直至第30天。第四组以与第三组相同的方式被注射MSG,并且以与第二组相同的方式被粉末处理。粉末的植物化学分析确定存在二烯丙基二硫化物,香芹酮,二烯丙基三硫化物和烯丙基四硫化物。 MSG引起的兴奋性毒性和认知缺陷表现为移动距离的缩短和在旷野中从中心开始移动需要很长时间,以及缺乏研究新颖物体和新颖手臂的好奇心。此外,味精会改变海马结构,并增加胶质纤维酸性蛋白(GFAP),钙网蛋白和caspase-3的MDA浓度和蛋白表达,而降低脑组织中的过氧化物歧化酶(SOD)活性和Ki-67的蛋白表达。然而,粉末通过增强抗氧化剂活性和减少脂质过氧化作用,阻止了味精诱导的神经毒性,并改善了短期记忆。此外,它降低了脑组织中GFAP,钙调蛋白和caspase-3的蛋白表达,并增加了Ki-67的蛋白表达,并保留了脑组织结构。这项研究表明,散剂可通过预防大鼠氧化应激诱导的神经胶质细胞增生和凋亡来改善味精对神经毒性的作用。

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