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Beneficial effects of PGC-1α in the substantia nigra of a mouse model of MPTP-induced dopaminergic neurotoxicity

机译:PGC-1α对MPTP诱发的多巴胺能神经毒性小鼠模型的黑质的有益作用

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摘要

Background: Mitochondrial dysfunction and oxidative stress are closely associated with the pathogenesis of Parkinson’s disease. Peroxisome proliferator-activated receptor γ coactivator 1 alpha (PGC-1α) is thought to play multiple roles in the regulation of mitochondrial biogenesis and cellular energy metabolism. We recently reported that altering PGC-1α gene expression modulates mitochondrial functions in N-methyl-4-phenylpyridinium ion (MPP ) treated human SH-SY5Y neuroblastoma cells, possibly via the regulation of Estrogen-related receptor α (ERRα), nuclear respiratory factor 1 (NRF-1), nuclear respiratory factor 2 (NRF-2) and peroxisome proliferator-activated receptor γ (PPARγ) expression. In the present study, we aimed to further investigate the potential beneficial effects of PGC-1α in the substantia nigra of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treated C57BL mice.
机译:背景:线粒体功能障碍和氧化应激与帕金森氏病的发病机理密切相关。过氧化物酶体增殖物激活受体γ共激活因子1 alpha(PGC-1α)被认为在线粒体生物发生和细胞能量代谢的调节中起多种作用。我们最近报道,改变PGC-1α基因表达可调节N-甲基-4-苯基吡啶鎓离子(MPP)治疗的人SH-SY5Y神经母细胞瘤细胞的线粒体功能,可能是通过调节雌激素相关受体α(ERRα),核呼吸因子1(NRF-1),核呼吸因子2(NRF-2)和过氧化物酶体增殖物激活受体γ(PPARγ)的表达。在本研究中,我们旨在进一步研究PGC-1α对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)治疗的C57BL小鼠黑质的潜在有益作用。

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