NecroX-5 protects mitochondrial oxidative phosphorylation capacity and preserves PGC1α expression levels during hypoxia/ reoxygenation injury
NecroX-5 protects mitochondrial oxidative phosphorylation capacity and preserves PGC1α expression levels during hypoxia/ reoxygenation injury
- Vu Thi Thu Hyoung Kyu Kim Le Thanh Long Bayalagmaa Nyamaa In-Sung Song To Thanh Thuy Nguyen Quang Hu
- 대한생리학회-대한약리학회
- The Korean Journal of Physiology & Pharmacology
- 제20권 제2호
- 등재여부 : KCI등재
- 2016.01
- 201 - 211 (11 pages)
Although the antioxidant and cardioprotective effects of NecroX-5 on various <i>in vitro</i> and<i> in vivo</i> 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 <i>ex vivo</i> 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.