Wenting Lu, Ping Liu, Haitao Jiao, Meng Qiao, Xiaofei Ren
Department of Hygiene Detection, College of Public Health, University of Shandong, Jinan, China.
Neurol Sci. 2014 Oct;35(10):1579-84. doi: 10.1007/s10072-014-1801-x. Epub 2014 Apr 27.
The aim of the study was to demonstrate the therapeutic effect of taurine against aluminum (Al)-induced neurological disorders in rats. Forty-two Wistar rats were randomly allotted into six groups: control (saline only), Al exposure (281.4 mg/kg/day for 1 month), Al + taurine (Al administration as previously plus taurine, doses were 200, 400 and 800 mg/kg/day, respectively, for the next 1 month) and prevention group (along with the Al administration as previously, 400 mg/kg/day taurine was treated for 1 month. During the next 1 month, rats were given taurine 400 mg/kg/day only). Starting from the sixth week, the body weight gain was significantly reduced in Al exposure group compared with saline (P < 0.05), and at the eighth week, the gain in prevention group was increased compared with Al (P < 0.05). Brain coefficient was gained in Al exposure compared with saline or prevention group (P < 0.05). Al exposure resulted in learning and memory impairment by increasing the escape latency and searching distance, meanwhile, decreasing the swimming time in the quadrant of platform and the numbers of crossing the platform (P < 0.05). Unsurprisingly, taurine treatment (400, 800 mg/kg/day and prevention) significantly protected against Al-induced brain dysfunction (P < 0.05). The Al exposure led to significant decreases in levels of γ-GABA and Tau, meanwhile, increased in level of Asp and Glu compared with saline (P < 0.05). And yet, taurine treatment partially reversed the deteriorated changes. The results suggested that taurine probably has neuroprotective effect against Al-induced learning, memory and brain neurotransmitters dysfunction.
本研究的目的是证明牛磺酸对铝（Al）诱导的大鼠神经功能障碍的治疗作用。42只Wistar大鼠被随机分为六组：对照组（仅给予生理盐水）、铝暴露组（281.4 mg/kg/天，持续1个月）、铝+牛磺酸组（先给予铝，剂量同前，随后1个月分别给予200、400和800 mg/kg/天的牛磺酸）和预防组（先给予铝，剂量同前，同时给予400 mg/kg/天的牛磺酸，持续1个月。接下来的1个月，仅给予大鼠400 mg/kg/天的牛磺酸）。从第六周开始，铝暴露组的体重增加量与生理盐水组相比显著降低（P<0.05），在第八周时，预防组的体重增加量与铝暴露组相比有所增加（P<0.05）。与生理盐水组或预防组相比，铝暴露组的脑系数增加（P<0.05）。铝暴露通过增加逃避潜伏期和搜索距离导致学习和记忆障碍，同时减少在平台象限的游泳时间和穿越平台的次数（P<0.05）。不出所料，牛磺酸治疗（400、800 mg/kg/天及预防组）显著预防了铝诱导的脑功能障碍（P<0.05）。与生理盐水组相比，铝暴露导致γ-氨基丁酸（γ-GABA）和微管相关蛋白tau（Tau）水平显著降低，同时天冬氨酸（Asp）和谷氨酸（Glu）水平升高（P<0.05）。然而，牛磺酸治疗部分逆转了这些恶化的变化。结果表明，牛磺酸可能对铝诱导的学习、记忆及脑神经递质功能障碍具有神经保护作用。
