کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2524971 1557968 2015 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
MicroRNA-214 participates in the neuroprotective effect of Resveratrol via inhibiting α-synuclein expression in MPTP-induced Parkinson’s disease mouse
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی تومور شناسی
پیش نمایش صفحه اول مقاله
MicroRNA-214 participates in the neuroprotective effect of Resveratrol via inhibiting α-synuclein expression in MPTP-induced Parkinson’s disease mouse
چکیده انگلیسی

Backgrounds and aimsMicroRNAs (miRNAs) have been reported to be involved in degenerative disorders including Parkinson’s disease (PD). α-synuclein expression is strong associated with the pathogenesis of PD. In the present study, we investigated whether the regulation of α-synuclein expression by miR-214 is the potential mechanism underlying the neuroprotective effect of Resveratrol.MethodsThe PD mouse model was established with the injection of MPTP (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and the human neuroblastoma cell line, SH-SY5Y, was administrated with MPP+.ResultsThe midbrain of PD mice and MPP+ treated SH-SY5Y cells had the lower expression levels of miR-214 and higher mRNA and protein expression of α-synuclein, which were reversed by Resveratrol administration. MiR-214 mimic down-regulated expression of α-synuclein and its 3′-UTR activity, while the levels were up-regulated by miR-214 inhibitor. In addition, the cell viability, elevated by Resveratrol, was also decreased by miR-214 inhibitor or overexpressed α-synuclein. In vivo, miR-214 inhibitor down-regulated TH+ cells of ipsilateral and up-regulated α-synuclein expression compared with the group treated with Resveratrol.ConclusionThe loss of miR-214 in PD resulted in the increase of α-synuclein expression, which was the potential mechanism underlying the neuroprotective effects of Resveratrol.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biomedicine & Pharmacotherapy - Volume 74, August 2015, Pages 252–256
نویسندگان
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