首页> 外文期刊>The Journal of Nutritional Biochemistry >Role of the inhibition of oxidative stress and inflammatory mediators in the neuroprotective effects of hydroxytyrosol in rat brain slices subjected to hypoxia reoxygenation.
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Role of the inhibition of oxidative stress and inflammatory mediators in the neuroprotective effects of hydroxytyrosol in rat brain slices subjected to hypoxia reoxygenation.

机译:氧化应激和炎性介质的抑制作用在低氧复氧大鼠脑片中羟基酪醇的神经保护作用中。

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摘要

The aim of this study was to analyze the mechanism of the neuroprotective effect of hydroxytyrosol (HT) in an experimental model of hypoxia-reoxygenation in rat brain slices. After reoxygenation the increase in lactate dehydrogenase efflux was inhibited by HT in a concentration-dependent manner and dose-dependent inhibition after oral administration to rats for 7 days (1, 5 and 10 mg/kg per day). Maximum inhibition was 57.4% in vitro and 38.7% ex vivo. Hydroxytyrosol reduced oxidative stress parameters: it inhibited lipid peroxidation and increased enzymatic activities related with the glutathione system both in vitro and after oral administration to rats. The increase in prostaglandin E2 and interleukin 1 beta after reoxygenation were inhibited after incubation of brain slices with HT and after oral administration. The accumulation of nitric oxide in brain slices was reduced in a concentration-dependent manner. In conclusion, HT exerts a neuroprotective effect in a model of hypoxia-reoxygenation in rat brain slices, both in vitro and after 7 days of oral administration to rats. HT exerts an antioxidant activity and lowered some inflammatory markers in this model
机译:这项研究的目的是分析羟基酪醇(HT)在大鼠脑片缺氧-复氧实验模型中的神经保护作用的机制。复氧后,口服给予大鼠7天(每天1、5和10 mg / kg)后,HT以浓度依赖的方式抑制乳酸脱氢酶外流的增加,并以剂量​​依赖的方式抑制。体外最大抑制为57.4%,离体最大抑制为38.7%。羟基酪醇降低了氧化应激参数:在体外和大鼠口服后,均能抑制脂质过氧化并增加与谷胱甘肽系统有关的酶活性。脑切片与HT孵育后和口服后,复氧后前列腺素E 2 和白介素1β的增加受到抑制。一氧化氮在脑片中的积累以浓度依赖的方式减少。总之,在大鼠体外和口服7天后,HT在大鼠脑片缺氧-复氧模型中发挥神经保护作用。 HT在该模型中发挥抗氧化作用并降低了一些炎症标记

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