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The protect role of nuclear respiratory factor 1 in mitochondrial damage in cardiac muscles |
QIN Guo-hua1,2, WANG Rui-xia1, XU Zhi-fang1,3, SANG Nan1 |
1. College of Environmental Science and Resources, Shanxi University, Taiyuan 030006, China;
2. Guangzhou Key Laboratory of Environmental Exposure and Health, School of Environment, Jinan University, Guangzhou 510632, China;
3. Shanxi Academy for Environmental Planning, Taiyuan 030001, China |
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Abstract We constructed a NRF1-pcDNA3.1 plasmid and transfected it in H9C2 cells to explore the effects of NRF1 in sodium bisulfite-induced mitochondrial damage in cardiac muscles of rats. H9C2 cells were treated with 100mmol/L NaHSO3 for 24h after NRF1-pcDNA3.1 or pcDNA3.1 transfection. Protein levels of NRF1 and TFAM were measured by Western blotting. The amount of ATP was detected by the chemiluminescence method. It showed that NaHSO3 treatment for 24h resulted in significant decreases of NRF1 and TFAM protein expression and ATP amount. The protein levels of NRF1 and TFAM were significantly elevated after NRF1-pcDNA3.1 plasmid transfection, companied by a significant increase of ATP amounts. NRF1and TFAM protein expressions and ATP amount significantly increased after NaHSO3 exposure for 24h in NRF1 over-expression group, compared with the pcDNA3.1-transfection group. It implied that over-expression of NRF1 might regulate TFAM to increase intracellular ATP production. In addition, over-expression of NRF1 alleviated the dysfunction of mitochondrial ATP caused by NaHSO3 exposure. NRF1 plays an important role in the regulation of NaHSO3-induced mitochondrial damage.
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Received: 21 July 2016
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