辅酶Q可诱导黑质线粒体解偶联，并在帕金森病灵长类动物模型中防止多巴胺能细胞丢失。

Coenzyme Q induces nigral mitochondrial uncoupling and prevents dopamine cell loss in a primate model of Parkinson's disease.

作者信息

Horvath Tamas L, Diano Sabrina, Leranth Csaba, Garcia-Segura Luis Miguel, Cowley Michael A, Shanabrough Marya, Elsworth John D, Sotonyi Peter, Roth Robert H, Dietrich Edwin H, Matthews Russel T, Barnstable Colin J, Redmond D Eugene

机构信息

Department of Obstetrics and Gynecology, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06520, USA.

出版信息

Endocrinology. 2003 Jul;144(7):2757-60. doi: 10.1210/en.2003-0163.

DOI:10.1210/en.2003-0163

PMID:12810526

Abstract

Parkinson's disease is characterized by dopamine cell loss of the substantia nigra. Parkinson's disease and the neurotoxin 1-methyl-4-phenyl-1,2,5,6 tetrahydropyridine may destroy dopamine neurons through oxidative stress. Coenzyme Q is a cofactor of mitochondrial uncoupling proteins that enhances state-4 respiration and eliminate superoxides. Here we report that short-term oral administration of coenzyme Q induces nigral mitochondrial uncoupling and prevents dopamine cell loss after 1-methyl-4-phenyl-1,2,5,6 tetrahydropyridine administration in monkeys.

摘要

帕金森病的特征是黑质多巴胺能细胞丢失。帕金森病和神经毒素1-甲基-4-苯基-1,2,5,6-四氢吡啶可能通过氧化应激破坏多巴胺能神经元。辅酶Q是线粒体解偶联蛋白的一种辅助因子，可增强状态4呼吸并清除超氧化物。在此我们报告，在猴子中，短期口服辅酶Q可诱导黑质线粒体解偶联，并预防1-甲基-4-苯基-1,2,5,6-四氢吡啶给药后多巴胺能细胞的丢失。