| 저자(한글) |
Vu, Thi Thu,Kim, Hyoung Kyu,Le, Thanh Long,Nyamaa, Bayalagmaa,Song, In-Sung,To, Thanh Thuy,Nguyen, Quang Huy,Marquez, Jubert,Kim, Soon Ha,Kim, Nari,Ko, Kyung Soo,Rhee, Byoung Doo,Han, Jin |
| 초록 |
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 ( $10{ mu}M$ ) 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 receptor-gamma coactivator- $1{ alpha}$ ( $PGC1{ alpha}$ ) 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 $PGC1{ alpha}$ during cardiac HR injuries. |
