Ikeda Katsumi, Negishi Hiroko, Yamori Yukio
School of Human Environmental Sciences, Mukogawa Women's University, Ikebiraki-cho, Nishinomiya, Japan.
Toxicology. 2003 Jul 15;189(1-2):55-61. doi: 10.1016/s0300-483x(03)00152-5.
Cerebral ischemia and recirculation cause delayed neuronal death in rodents, such as Mongolian gerbils and stroke-prone spontaneously hypertensive rats (SHRSP), which were used as an experimental stroke model. It was documented that an enhanced nitric oxide production, the occurrence of apoptosis, and an attenuated redox regulatory system contribute to the development of delayed neuronal death. Many studies have suggested the beneficial antioxidant effects of antioxidant nutrients such as vitamin E, green tea extract, ginkgo biloba extract, resveratrol and niacin in cerebral ischemia and recirculation brain injury. These results are important in light of an attenuation of the deleterious consequences of oxidative stress in ischemia and recirculation injury.
脑缺血再灌注会导致啮齿动物(如蒙古沙鼠和易患中风的自发性高血压大鼠(SHRSP),它们被用作实验性中风模型)出现迟发性神经元死亡。据记载,一氧化氮生成增加、细胞凋亡的发生以及氧化还原调节系统减弱都有助于迟发性神经元死亡的发展。许多研究表明,抗氧化营养素如维生素E、绿茶提取物、银杏叶提取物、白藜芦醇和烟酸在脑缺血再灌注脑损伤中具有有益的抗氧化作用。鉴于这些结果能够减轻缺血再灌注损伤中氧化应激的有害后果,所以它们具有重要意义。