机译:噻唑烷二酮治疗通过诱导性一氧化氮合酶介导的脂质自由基形成而减轻自发性高血压心力衰竭大鼠的氧化应激
Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina;
Section of Cardiology, Department of Pharmacology, University of Illinois, Chicago, Illinois;
Oxidative Stress and Disease Laboratory, Gene-Nutrient Interaction Laboratory, Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana;
Oxidative Stress and Disease Laboratory, Gene-Nutrient Interaction Laboratory, Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana;
Oxidative Stress and Disease Laboratory, Gene-Nutrient Interaction Laboratory, Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana;
Oxidative Stress and Disease Laboratory, Gene-Nutrient Interaction Laboratory, Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana;
机译:性别对自发性高血压大鼠心脏和大脑的氧化应激,脂质过氧化,蛋白质损伤和细胞凋亡的影响。
机译:一氧化氮,血管紧张素II和超氧化物歧化酶对自发性高血压大鼠运动引起的血压升高衰减的作用
机译:一氧化氮合酶介导的一氧化氮早期爆发减轻了水分胁迫引起的铵根供应的水稻根系的氧化损伤
机译:一氧化氮在自发性高血压大鼠中介导可溶性可可纤维产品的抗高血压和血管松弛作用
机译:一氧化氮从微血管和大冠状动脉形成/释放的机制以及充血性心力衰竭释放中的变化
机译:噻唑烷二酮治疗通过诱导性一氧化氮合酶介导的脂质自由基形成而减轻自发性高血压心力衰竭大鼠的氧化应激
机译:噻唑烷二酮处理通过诱导型一氧化氮合酶介导的脂质自由基形成,降低自发性高血压性心力衰竭大鼠的氧化应激