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Cell Journal، جلد ۲۱، شماره ۱، صفحات ۱-۶
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عنوان انگلیسی 17 β-Estradiol Oxidative Stress Attenuation and Autophagy-Induced Dopaminergic Neuroprotection
چکیده انگلیسی مقاله Objective: Dopaminergic neurons in the substantia nigra of the brain stem are the main pathological aspect of Parkinson's disease. 17 β-estradiol (E2) has neuroprotective effects on substantia nigra, however, the underlined mechanism is not well-known. In this study, we evaluated the neuroprotective effects of E2 in the ovariectomized 6-hydroxydopamine- (6-OHDA) rat model of PD. Materials and methods: At first, all the animals were ovariectomized for any further bias in the E2 levels and then these ovariectomized rats were randomly assigned into three experimental groups (10 rats in each group): ovariectomized control group (OCG), ovariectomized degeneration group receiving 25 μg of 6-OHDA into the left corpus striatum (ODG), and ovariectomized E2 pretreatment rats were (pretreated with 0.1 mg kg-1 of 17 β-estradiol for three days prior to the destruction of corpus striatum with 6-OHDA (OE2PTG). The behavioral test was performed using apomorphine. The expressions of Sequestosome-1 (p62), Unc- 51 like autophagy activating kinase (ULK1) and Microtubule-associated proteins 1A/1B light chain 3B (LC3) genes were evaluated using RT- PCR. Moreover, the reactive oxygen species and malondialdehyde levels in the midbrain were assessed. Results: In the treatment group, 6-OHDA increased reactive oxygen species and malondialdehyde levels and E2 reduced this damages to dopaminergic neurons of the substantia nigra as the motor behavior and the number of rotations and also histological tests in the treatment group showed cell survival improvements as compared to the control groups; indicating E2 neurodegeneration prevention in the substantia nigra. Moreover, P62 and LC3 expressed in all of the experimental groups while ULK1 did not express in the ODG group meanwhile ULK1 expressed after treating with E2 in the OE2PTG group. Conclusion: E2 prevents midbrain dopaminergic neurons degeneration by ULK1 gene overexpression and augmenting autophagy.
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نویسندگان مقاله | Roya Varmazyar


| Ali Noori-Zadeh


| Farzad Rajaei


| Shahram Darabi


| Salar Bakhtiyari


نشانی اینترنتی http://celljournal.org/journal/article/abstract/5799
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