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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Chronic treatment with taurine after intracerebroventricular streptozotocin injection improves cognitive dysfunction in rats by modulating oxidative stress, cholinergic functions and neuroinflammation
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Chronic treatment with taurine after intracerebroventricular streptozotocin injection improves cognitive dysfunction in rats by modulating oxidative stress, cholinergic functions and neuroinflammation

机译:通过调节氧化应激,胆碱能功能和神经炎,患有牛磺酸后的牛磺酸慢性治疗改善了大鼠的认知功能障碍

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摘要

The present study investigated the neuroprotective effects of taurine, an essential amino acid for growth and development of central nervous system. Intracerebroventricular streptozotocin (ICV-STZ) model of cognitive impairment was used in male Wistar rats (270 +/- 20 g). Morris water maze, elevated plus maze and passive avoidance paradigm were used to assess cognitive performance. Taurine (40, 60 and 120 mg/kg) was administered orally for 28 days following STZ administration on day 1. Oxidative stress parameters (malondialdehyde, glutathione, nitric oxide and superoxide dismutase) and cholinesterases (acetylcholinesterase and butyrylcholinesterase) activity were measured at end of the study in the cortex and hippocampus. Levels of TNF-alpha, IL-1 beta, expression of rho kinase-II (ROCK-II), glycogen synthase kinase-3 beta (GSK-3 beta) and choline acetyltransferase (ChAT) were studied in cortex and hippocampus. STZ caused significant cognitive impairment as compared to normal control. Chronic administration of taurine attenuated STZ-induced cognitive impairment. Increased oxidative stress and increased levels of TNF-alpha, IL-1 beta induced by STZ were also significantly attenuated by taurine. Taurine significantly (p < 0.05) decreased the STZ-induced increased expression of ROCK-II in cortex and hippocampus. Further, STZ-induced increased activity of cholinesterases was significantly (p < 0.001) mitigated by taurine. STZ decreased the expression of ChAT in hippocampus which was significantly (p < 0.05) reversed by taurine. However, GSK-3 beta expression was not altered by either STZ or taurine. The present study indicates that taurine exerts a neuroprotective role against STZ-induced cognitive impairment in rats. This effect is probably mediated by modulating oxidative stress, cholinesterases, inflammatory cytokines and expression of ROCK-II. Thus, this study suggests a potential of chronic taurine administration in cognitive impairment of Alzheimer's type. (C) 2017 Elsevier Ltd. All rights reserved.
机译:本研究研究了牛磺酸的神经保护作用,是一种中枢神经系统生长和发育的必需氨基酸。在雄性Wistar大鼠(270 +/-20g)中使用认知障碍的颅内腔内链霉菌(ICV-STZ)模型。 Morris水迷宫,升高的加迷宫和被动避免范式用于评估认知性能。在STZ给药后,在STZ给药后牛磺酸(40,60和120mg / kg)在第1天后进行28天。在结束时测量氧化应激参数(丙炔,谷胱甘肽,一氧化氮和超氧化物歧化酶(乙酰胆碱酯酶和丁酰基胆碱酯酶)活性在皮质和海马研究中的研究。在皮质和海马中,研究了TNF-1β,rhO-1β,rhO激酶-II(ROCK-II),糖原合酶激酶-3β(GSK-3β)和胆碱乙酰转移酶(聊天)的水平。与正常对照相比,STZ引起了显着的认知障碍。牛磺酸的慢性施用减弱了STZ引起的认知障碍。增加的氧化应激和TNF-α的水平增加,STZ诱导的IL-1β也被牛磺酸显着减弱。牛磺酸显着(P <0.05)降低了STZ诱导的皮质和海马岩体岩体的表达。此外,STZ诱导的胆碱酯酶的增加的活性显着(p <0.001)被牛磺酸减轻。 STZ降低了在海马中的聊天表达,这是显着的(P <0.05)的牛磺酸逆转。然而,通过STZ或牛磺酸不会改变GSK-3β表达。本研究表明,牛磺酸对大鼠的抗STZ诱导的认知障碍发挥神经保护作用。这种效果可能是通过调节氧化应激,胆碱酶,炎性细胞因子和岩石-II的表达来介导的。因此,本研究表明,慢性牛磺酸局在阿尔茨海默氏症类型的认知障碍中的潜力。 (c)2017 Elsevier Ltd.保留所有权利。

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