重组人线粒体转录因子 A 可刺激线粒体生物发生和 ATP 合成，改善 MPTP 后运动功能，减少氧化应激，增加内毒素后存活率。
Recombinant human mitochondrial transcription factor A stimulates mitochondrial biogenesis and ATP synthesis, improves motor function after MPTP, reduces oxidative stress and increases survival after endotoxin.
机构信息
Morris Udall Parkinson's Disease Research Center of Excellence, University of Virginia, Charlottesville, VA, United States.
出版信息
Mitochondrion. 2011 Jan;11(1):108-18. doi: 10.1016/j.mito.2010.08.004. Epub 2010 Aug 18.
Abstract
Recombinant human mitochondrial transcription factor A protein (rhTFAM) was evaluated for its acute effects on cultured cells and chronic effects in mice. Fibroblasts incubated with rhTFAM acutely increased respiration in a chloramphenicol-sensitive manner. SH-SY5Y cells showed rhTFAM concentration-dependent reduction of methylpyridinium (MPP(+))-induced oxidative stress and increases in lowered ATP levels and viability. Mice treated with weekly i.v. rhTFAM showed increased mitochondrial gene copy number, complex I protein levels and ATP production rates; oxidative damage to proteins was decreased ~50%. rhTFAM treatment improved motor recovery rate after treatment with MPTP and dose-dependently improved survival in the lipopolysaccharide model of endotoxin sepsis.
摘要
重组人线粒体转录因子 A 蛋白 (rhTFAM) 已被评估其对培养细胞的急性作用和对小鼠的慢性作用。与 rhTFAM 孵育的成纤维细胞可迅速以氯霉素敏感的方式增加呼吸作用。SH-SY5Y 细胞表现出 rhTFAM 浓度依赖性降低甲基吡啶鎓 (MPP(+)) 诱导的氧化应激和降低的 ATP 水平和活力增加。每周静脉注射 rhTFAM 的小鼠表现出线粒体基因拷贝数增加，复合物 I 蛋白水平和 ATP 产生速率增加；蛋白质的氧化损伤减少了约 50%。rhTFAM 治疗可改善 MPTP 治疗后的运动恢复率，并在脂多糖内毒素败血症模型中剂量依赖性地改善生存。
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