抑制Sirtuin 2可减少幼时摄入高铁大鼠衰老后纹状体神经元多巴胺耗竭_非多巴胺能神经元
抑制Sirtuin 2可减少幼时摄入高铁大鼠衰老后纹状体神经元多巴胺耗竭由刀豆文库小编整理，希望给你工作、学习、生活带来方便，猜你可能喜欢“非多巴胺能神经元”。
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作者：汪锡金
稿号：NRR-D-14-00281 抑制Sirtuin 2可减少幼时摄入高铁大鼠衰老后纹状体神经元多巴胺耗竭
铁是人体必需的微量元素，能参与电子转移、氧运输、神经递质合成和中枢神经系统髓鞘生成的过程，且铁代谢受损可能损害神经元，特别是多巴胺能神经元。因此铁失衡被认为与帕金森病的发病机制有关，新生儿铁摄入对成年及衰老的长期影响已经引起许多研究者的兴趣。幼时高铁能增加其出现帕金森病等衰老相关的神经退行性疾病的后果。
来自中国上海交通大学医学院附属新华医院的汪锡金所在团队，观察到在幼时高铁(120 µg/g/d)灌胃的大鼠，与未摄入高铁大鼠相比，衰老后出现明显的行为异常和纹状体多巴胺耗竭。AK-7是一种可渗透细胞和大脑的选择性Sirtuin 2抑制剂，被用来研究Sirtuin 2抑制对幼时高铁摄入衰老大鼠纹状体神经元多巴胺耗竭和行为异常的影响。实验每日均为双侧黑质内注射5µg/d的Sirtuin 2抑制剂AK-7，可显著改善幼时高铁摄入的衰老大鼠纹状体神经元中多巴胺耗竭及行为异常。
作者实验结果表明，大鼠幼时高铁摄入会导致衰老后出现帕金森病样的神经化学和行为变化，而抑制Sirtuin 2表达可对其产生神经保护作用。相关文献发表于《中国神经再生研究（英文版）》杂志2014年11月第21期。
Article: “ Inhibition of Sirtuin 2 exerts neuroprotection in aging rats with increased neonatal iron intake,” by Xijin Wang1, Meihua Wang1, Liu Yang1, Jie Bai1, Zhiqiang Yan2, Yuhong Zhang3, Zhenguo Liu1(1 Department of Neurology, Xinhua Hospital Affliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China;2 Shanghai Laboratory Animal Center, Chinese Academy of Sciences, Shanghai, China;3 Department of Neurology, Shanghai Tenth People’s Hospital, Tongji University, Shanghai, China)
Wang XJ, Wang MH, Yang L, Bai J, Yan ZQ, Zhang YH, Liu ZG.Inhibition of Sirtuin 2 exerts neuroprotection in aging rats with increased neonatal iron intake.Neural Regen Res.2014;9(21):1917-1922.欲获更多资讯： Neural Regen Res
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作者：汪锡金
稿号：NRR-D-14-00281 Inhibition of Sirtuin 2 reduces striatal dopamine depletion in aging rats with increased neonatal iron intake Iron is an eential trace metal.It plays an important role in electron transfer, oxygen transport, neurotransmitter synthesis, and myelin production in the central nervous system.However, impaired iron homeostasis may be harmful to neurons, especially dopaminergic neurons.Iron dyshomeostasis is aociated with the etiopathogenesis of Parkinson’s disease.It is of interest to investigate the long-ranging effects of neonatal iron intake in adulthood and senescence.Elevated neonatal iron intake in mice contributed to age-related neurodegeneration similar to Parkinson’s disease.Xijin Wang, at Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, China and his colleagues found that neonatal iron intake(120 µg/g per day)during postnatal days 10–17 resulted in significant behavior abnormalities and striatal dopamine depletion in aging rats compared to those without iron intake.After AK-7, a selective Sirtuin 2 inhibitor, was injected into the substantia nigra at postnatal 540 days and 570 days(5 µg/side per day), striatal dopamine depletion was significantly diminished and behavior abnormality was improved in aging rats with neonatal iron intake.Experimental findings suggest that increased neonatal iron intake may result in Parkinson’s disease-like neurochemical and behavioral deficits with aging, and inhibition of Sirtuin 2 expreion may be a neuroprotective measure in Parkinson’s disease.These results were published in Neural Regeneration Research(Vol.9, No.21, 2014).Article: “ Inhibition of Sirtuin 2 exerts neuroprotection in aging rats with increased neonatal iron intake,” by Xijin Wang1, Meihua Wang1, Liu Yang1, Jie Bai1, Zhiqiang Yan2, Yuhong Zhang3, Zhenguo Liu1(1 Department of Neurology, Xinhua Hospital Affliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China;2 Shanghai Laboratory Animal Center, Chinese Academy of Sciences, Shanghai, China;3 Department of Neurology, Shanghai Tenth People’s Hospital, Tongji University, Shanghai, China)
Wang XJ, Wang MH, Yang L, Bai J, Yan ZQ, Zhang YH, Liu ZG.Inhibition of Sirtuin 2 exerts neuroprotection in aging rats with increased neonatal iron intake.Neural Regen Res.2014;9(21):1917-1922.
