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牛磺酸治疗可提供锰中毒小鼠模型的神经保护。

Taurine Treatment Provides Neuroprotection in a Mouse Model of Manganism.

机构信息

Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, P. O. Box 158371345, Roknabad, Karafarin St., Shiraz, Fars, Iran.

Department of Pharmacology and Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran.

出版信息

Biol Trace Elem Res. 2019 Aug;190(2):384-395. doi: 10.1007/s12011-018-1552-2. Epub 2018 Oct 24.

Abstract

Manganese (Mn) is a trace element involved in many physiological processes. However, excessive Mn exposure leads to neurological complications. Although no precise mechanism(s) has been found for Mn-induced neurotoxicity, oxidative stress and mitochondrial injury seem to play a relevant role in this complication. On the other hand, there is no protective strategy against Mn neurotoxicity so far. Taurine is an amino acid with significant neuroprotective properties. The current study was designed to evaluate the effect of taurine supplementation and its potential mechanism(s) of action in a mouse model of manganism. Animals were treated with Mn (100 mg/kg, s.c) alone and/or in combination with taurine (50, 100, and 500 mg/kg, i.p, for eight consecutive days). Severe locomotor dysfunction along with a significant elevation in brain tissue biomarkers of oxidative stress was evident in Mn-exposed mice. On the other hand, it was revealed that mitochondrial indices of functionality were hampered in Mn-treated animals. Taurine supplementation (50, 100, and 500 mg/kg, i.p) alleviated Mn-induced locomotor deficit. Moreover, this amino acid mitigated oxidative stress biomarkers and preserved brain tissue mitochondrial indices of functionality. These data introduce taurine as a potential neuroprotective agent against Mn neurotoxicity. Antioxidative and mitochondria protecting effects of taurine might play a fundamental role in its neuroprotective properties against Mn toxicity.

摘要

锰(Mn)是一种参与许多生理过程的微量元素。然而,过量的锰暴露会导致神经并发症。虽然尚未发现锰诱导的神经毒性的确切机制,但氧化应激和线粒体损伤似乎在这一并发症中起相关作用。另一方面,目前尚无针对锰神经毒性的保护策略。牛磺酸是一种具有重要神经保护特性的氨基酸。本研究旨在评估牛磺酸补充剂对锰中毒小鼠模型的作用及其潜在作用机制。动物单独用 Mn(100mg/kg,sc)处理和/或并用牛磺酸(50、100 和 500mg/kg,ip,连续 8 天)处理。暴露于 Mn 的小鼠表现出严重的运动功能障碍,以及脑组织氧化应激生物标志物的显著升高。另一方面,研究表明 Mn 处理动物的线粒体功能指数受到阻碍。牛磺酸补充剂(50、100 和 500mg/kg,ip)缓解了 Mn 诱导的运动缺陷。此外,这种氨基酸减轻了氧化应激生物标志物,并保护了脑组织线粒体功能的指数。这些数据表明牛磺酸是一种潜在的神经保护剂,可对抗锰神经毒性。牛磺酸的抗氧化和保护线粒体作用可能在其对抗锰毒性的神经保护特性中起重要作用。

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