Abstract Title:

Water-Soluble Coenzyme Q10 Reduces Rotenone-Induced Mitochondrial Fission.

Abstract Source:

Neurochem Res. 2017 Apr ;42(4):1096-1103. Epub 2017 Feb 11. PMID: 28190227

Abstract Author(s):

Hai-Ning Li, Mary Zimmerman, Gaolin Z Milledge, Xiao-Lin Hou, Jiang Cheng, Zhen-Hai Wang, P Andy Li

Article Affiliation:

Hai-Ning Li


Parkinson's disease is a neurodegenerative disorder characterized by mitochondrial dysfunction and oxidative stress. It is usually accompanied by an imbalance in mitochondrial dynamics and changes in mitochondrial morphology that are associated with impaired function. The objectives of this study were to identify the effects of rotenone, a drug known to mimic the pathophysiology of Parkinson's disease, on mitochondrial dynamics. Additionally, this study explored the protective effects of water-soluble Coenzyme Q10 (CoQ10) against rotenone-induced cytotoxicity in murine neuronal HT22 cells. Our results demonstrate that rotenone elevates protein expression of mitochondrial fission markers, Drp1 and Fis1, and causes an increase in mitochondrial fragmentation as evidenced through mitochondrial staining and morphological analysis. Water-soluble CoQ10 prevented mitochondrial dynamic imbalance by reducing Drp1 and Fis1 protein expression to pre-rotenone levels, as well as reducing rotenone treatment-associated mitochondrial fragmentation. Hence, water-soluble CoQ10 may have therapeutic potential in treating patients with Parkinson's disease.

Study Type : In Vitro Study

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