Neurotoxicology Laboratory, Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi, 110062, India.
Neurol Sci. 2013 Dec;34(12):2181-92. doi: 10.1007/s10072-013-1444-3. Epub 2013 May 17.
Oxidative loads in the brain are involved in age related impairments like learning and memory as well as neurodegeneration. Taurine, the most abundant free amino acid in humans has many potential health benefits through its anti-oxidant and anti-inflammatory properties. Therefore, we investigated the neuroprotective potential of taurine on oxidative stress, neuronal loss and memory impairments in streptozotocin model of cognitive impairments in rats. The cognitive impairment was developed by giving single intracerebroventricular (ICV) injection of streptozotocin (STZ) 3 mg/kg body weight bilaterally. An increased latency and path length was observed in ICV-STZ group animals as compared to sham group animals and these were inhibited significantly in STZ group pre-treated with taurine (50 mg/kg body weight orally once daily for 15 days). Moreover, the significantly depleted content of GSH and elevated level of thiobarbituric acid reactive substances (TBARS) in ICV-STZ group animals were protected significantly with pre-treatment of taurine. The activity of antioxidant enzymes, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, catalase, and superoxide dismutase was decreased in STZ group as compared to sham group and pre-treatment of STZ group with taurine has protected their activities significantly. Furthermore, the increased activity of acetylcholine esterase and decreased expression of choline acetyl transferase were attenuated by the pre-treatment of taurine. Taurine also protected the morphology of the hippocampal pyramidal neurons. This study concludes that the prophylactic intervention of taurine may be used to prevent the deterioration of cognitive functions and neurobehavioral activities, often associated with the generation of free radicals.
大脑中的氧化负荷与年龄相关的损伤有关,如学习和记忆以及神经退行性变。牛磺酸是人类最丰富的游离氨基酸,具有抗氧化和抗炎特性,具有许多潜在的健康益处。因此,我们研究了牛磺酸对氧化应激、神经元丢失和记忆损伤的神经保护潜力,在链脲佐菌素诱导的认知损伤大鼠模型中。认知损伤是通过双侧脑室内(ICV)注射链脲佐菌素(STZ)3mg/kg 体重来诱导的。与假手术组动物相比,ICV-STZ 组动物的潜伏期和路径长度增加,而用牛磺酸(50mg/kg 体重,每天口服一次,共 15 天)预处理的 STZ 组动物的潜伏期和路径长度显著抑制。此外,ICV-STZ 组动物的 GSH 含量明显减少,TBARS 水平升高,用牛磺酸预处理可显著保护。与假手术组相比,STZ 组的抗氧化酶谷胱甘肽过氧化物酶、谷胱甘肽还原酶、谷胱甘肽-S-转移酶、过氧化氢酶和超氧化物歧化酶的活性降低,用牛磺酸预处理可显著保护其活性。此外,牛磺酸预处理可减轻乙酰胆碱酯酶活性的增加和胆碱乙酰转移酶表达的降低。牛磺酸还保护海马锥体神经元的形态。这项研究的结论是,牛磺酸的预防性干预可能用于预防认知功能和神经行为活动的恶化,这些活动通常与自由基的产生有关。