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KMID : 0811720160200020201
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Korean Journal of Physiology & Pharmacology
2016 Volume.20 No. 2 p.201 ~ p.211
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NecroX-5 protects mitochondrial oxidative phosphorylation capacity and preserves PGC1α expression levels during hypoxia/ reoxygenation injury
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Vu Thi Thu
Kim Hyoung-Kyu
Le Thanh Long
Bayalagmaa Nyamaa
Song In-Sung
To Thanh Thuy
Nguyen Quang Huy
Jubert Marquez
Kim Na-Ri
Kim Soon-Ha
Ko Kyung-Soo
Rhee Byoung-Doo
Han Jin
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Abstract
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Although the antioxidant and cardioprotective effects of NecroX-5 on various in vitro and in vivo models have been demonstrated, the action of this compound on the mitochondrial oxidative phosphorylation system remains unclear. Here we verify the role of NecroX-5 in protecting mitochondrial oxidative phosphorylation capacity during hypoxia-reoxygenation (HR). Necrox-5 treatment (10 μM) and non-treatment were employed on isolated rat hearts during hypoxia/ reoxygenation treatment using an ex vivo Langendorff system. Proteomic analysis was performed using liquid chromatography-mass spectrometry (LC-MS) and non-labeling peptide count protein quantification. Real-time PCR, western blot, citrate synthases and mitochondrial complex activity assays were then performed to assess heart function. Treatment with NecroX-5 during hypoxia significantly preserved electron transport chain proteins involved in oxidative phosphorylation and metabolic functions. NecroX-5 also improved mitochondrial complex I, II, and V function. Additionally, markedly higher peroxisome proliferator-activated receptorgamma coactivator-1α (PGC1α) expression levels were observed in NecroX-5-treated rat hearts. These novel results provide convincing evidence for the role of NecroX-5 in protecting mitochondrial oxidative phosphorylation capacity and in preserving PGC1α during cardiac HR injuries.
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KEYWORD
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Hypoxia, Mitochondria, NecroX, Oxidative phosphorylation, PCG1α
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