کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5827705 | 1558936 | 2014 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Epigenetic upregulation of alpha-synuclein in the rats exposed to methamphetamine
ترجمه فارسی عنوان
تنظیم مقادیر اپی ژنتیکی آلفا سینوکلین در موشهای تحت درمان با متامفتامین
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب سلولی و مولکولی
چکیده انگلیسی
Abuse of methamphetamine (METH) increases the risk of occurrence of Parkinson׳s disease (PD) in the individuals. Increased expression of synaptic protein α-synuclein (encoded by gene Snca) is remarkably associated with the neuronal loss and motor dysfunction in the patients with PD. The present study aimed to explore the epigenetic mechanism underlying the altered expression of α-synuclein in substantia nigra in the rats previously exposed to METH. Exposure to METH induced significant behavioral impairments in the rotarod test and open field test, as well as the upregulation of cytokine synthesis in the substantia nigra. Significantly increased expression of α-synuclein was also observed in the substantia nigra in the rats exposed to METH. Further chromatin immunoprecipitation and bisulfite sequencing studies revealed a significantly decreased cytosine methylation in the Snca promoter region in the rats exposed to METH. It was found that the occupancy of methyl CpG binding protein 2 and DNA methyltransferase 1 in Snca promoter region was also significantly decreased in the substantia nigra in the modeled rats. These results advanced our understanding on the mechanism of the increased incidence of PD in the individuals with history use of METH, and shed novel lights on the development of therapeutic approaches for the patients conflicted with this neurological disorder.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: European Journal of Pharmacology - Volume 745, 15 December 2014, Pages 243-248
Journal: European Journal of Pharmacology - Volume 745, 15 December 2014, Pages 243-248
نویسندگان
Wenda Jiang, Ji Li, Zhuang Zhang, Hongxin Wang, Zhejian Wang,