Lu Cai-Ling, Tang Shen, Meng Zhi-Juan, He Yi-Yuan, Song Ling-Yong, Liu Yin-Pin, Ma Ning, Li Xi-Yi, Guo Song-Chao
Department of Food and Nutrition, School of Public Health, Guangxi Medical University, 22 Shuangyong Road, 530021 Nanning, Guangxi, P,R, China.
J Biomed Sci. 2014 May 24;21(1):51. doi: 10.1186/1423-0127-21-51.
Excessive manganese exposure induced cognitive deficit. Several lines of evidence have demonstrated that taurine improves cognitive impairment induced by numerous neurotoxins. However, the role of taurine on manganese-induced damages in learning and memory is still elusive. This goal of this study was to investigate the beneficial effect of taurine on learning and memory capacity impairment by manganese exposure in an animal model.
The escape latency in the Morris Water Maze test was significantly longer in the rats injected with manganese than that in the rats received both taurine and manganese. Similarly, the probe trial showed that the annulus crossings were significantly greater in the taurine plus manganese treated rats than those in the manganese-treated rats. However, the blood level of manganese was not altered by the taurine treatment. Interestingly, the exposure of manganese led to a significant increase in the acetylcholinesterase activity and an evidently decrease in the choline acetyltransferase activity, which were partially restored by the addition of taurine. Additionally, we identified 9 differentially expressed proteins between the rat hippocampus treated by manganese and the control or the manganese plus taurine in the proteomic analysis using the 2-dimensional gel electrophoresis followed by the tandem mass spectrometry (MS/MS). Most of these proteins play a role in energy metabolism, oxidative stress, inflammation, and neuron synapse.
In summary, taurine restores the activity of AChE and ChAT, which are critical for the regulation of acetylcholine. We have identified seven differentially expressed proteins specifically induced by manganese and two proteins induced by taurine from the rat hippocampus. Our results support that taurine improves the impaired learning and memory ability caused by excessive exposure of manganese.
过量接触锰会导致认知缺陷。多项证据表明,牛磺酸可改善多种神经毒素所致的认知障碍。然而,牛磺酸在锰诱导的学习和记忆损伤中的作用仍不明确。本研究的目的是在动物模型中探究牛磺酸对锰暴露所致学习和记忆能力损伤的有益作用。
在莫里斯水迷宫试验中,注射锰的大鼠的逃避潜伏期显著长于同时接受牛磺酸和锰的大鼠。同样,探索性试验表明,牛磺酸加锰处理的大鼠穿越环的次数显著多于锰处理的大鼠。然而,牛磺酸处理并未改变血液中的锰水平。有趣的是,锰暴露导致乙酰胆碱酯酶活性显著增加,胆碱乙酰转移酶活性明显降低,而添加牛磺酸可部分恢复这些变化。此外,在二维凝胶电泳后进行串联质谱(MS/MS)的蛋白质组学分析中,我们鉴定出了锰处理的大鼠海马体与对照组或锰加牛磺酸处理组之间9种差异表达的蛋白质。这些蛋白质大多在能量代谢、氧化应激、炎症和神经元突触中发挥作用。
综上所述,牛磺酸可恢复对乙酰胆碱调节至关重要的乙酰胆碱酯酶和胆碱乙酰转移酶的活性。我们从大鼠海马体中鉴定出了7种由锰特异性诱导的差异表达蛋白质和2种由牛磺酸诱导的蛋白质。我们的结果支持牛磺酸可改善过量接触锰所致的学习和记忆能力损伤。