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N-乙酰半胱氨酸减轻1-甲基-4-苯基-1,2,3,6-四氢吡啶诱导的小鼠黑质纹状体毒性。

Attenuation of 1-methyl-4-phenyl-1, 2,3,6-tetrahydropyridine induced nigrostriatal toxicity in mice by N-acetyl cysteine.

作者信息

Sharma A, Kaur P, Kumar V, Gill K D

机构信息

Department of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, India.

出版信息

Cell Mol Biol (Noisy-le-grand). 2007 Apr 15;53(1):48-55.

Abstract

The present study was designed to investigate the effects of N-acetyl cysteine (NAC), an antioxidant on 1-methyl 4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) induced neurotoxicity in the nigrostriatal dopaminergic system of mice. MPTP treatment caused 80% decrease of the dopamine levels in the striatum of C57BL/ 6J mice. A marked increase in the extent of lipid peroxidation, superoxide dismutase (SOD) and g-glutamyl transpeptidase (g-GTP) was seen, while a significant decrease in the levels of glutathione (GSH), total thiols and glutathione peroxidase (GPx) activity was observed in the substantia nigra pars compacta (SNpc) of MPTP treated animals. As compared to control animals, Co-administration of NAC with MPTP restored the depleted dopamine, GSH, total tissue thiol levels and GPx activity in SNpc of treated mice brain. Moreover, NAC treatment also provided protection against lipid peroxidation and superoxide dismutase activity. The results of present study suggested that NAC attenuates MPTP neurotoxicity in mice brain and this protection by the NAC might be contributing to the regeneration of GSH, a major antioxidant.

摘要

本研究旨在探讨抗氧化剂N-乙酰半胱氨酸(NAC)对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的小鼠黑质纹状体多巴胺能系统神经毒性的影响。MPTP处理导致C57BL/6J小鼠纹状体中多巴胺水平降低80%。在MPTP处理动物的黑质致密部(SNpc)中,脂质过氧化程度、超氧化物歧化酶(SOD)和γ-谷氨酰转肽酶(γ-GTP)显著增加,而谷胱甘肽(GSH)、总硫醇水平和谷胱甘肽过氧化物酶(GPx)活性显著降低。与对照动物相比,NAC与MPTP共同给药可恢复处理小鼠脑SNpc中耗尽的多巴胺、GSH、总组织硫醇水平和GPx活性。此外,NAC处理还能防止脂质过氧化和超氧化物歧化酶活性。本研究结果表明,NAC可减轻小鼠脑中MPTP的神经毒性,NAC的这种保护作用可能有助于主要抗氧化剂GSH的再生。

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