UC知道帮我翻译一篇医学方面的文章，谢啦~~~
来源：百度知道 编辑：UC知道 时间：2024/05/22 02:53:14
以下是美国国立图书馆的一篇文章，是有关缺血再灌注损伤的：
Transcription factor Nrf2 is protective during ischemic and nephrotoxic acute kidney injury in mice.
Oxidative stress is involved in acute kidney injury due to ischemia-reperfusion and chemotherapy-induced nephrotoxicity. To investigate their basic mechanisms we studied the role of nuclear factor-erythroid 2-p45-related factor 2 (Nrf2), a redox-sensitive transcription factor that regulates expression of several antioxidant and cytoprotective genes. We compared the responses of Nrf2-knockout mice and their wild-type littermates in established mouse models of ischemia-reperfusion injury and cisplatin-induced nephrotoxicity. Several Nrf2-regulated genes encoding antioxidant enzymes/proteins were significantly upregulated in the kidneys of wild type but not Nrf2-knockout mice following renal ischemia. Renal function, histology, vascular permeability, and survival were each significantly worse in the Nrf2 knockout mice. Further, proinflammatory cytokin
Transcription factor Nrf2 is protective during ischemic and nephrotoxic acute kidney injury in mice.
Oxidative stress is involved in acute kidney injury due to ischemia-reperfusion and chemotherapy-induced nephrotoxicity. To investigate their basic mechanisms we studied the role of nuclear factor-erythroid 2-p45-related factor 2 (Nrf2), a redox-sensitive transcription factor that regulates expression of several antioxidant and cytoprotective genes. We compared the responses of Nrf2-knockout mice and their wild-type littermates in established mouse models of ischemia-reperfusion injury and cisplatin-induced nephrotoxicity. Several Nrf2-regulated genes encoding antioxidant enzymes/proteins were significantly upregulated in the kidneys of wild type but not Nrf2-knockout mice following renal ischemia. Renal function, histology, vascular permeability, and survival were each significantly worse in the Nrf2 knockout mice. Further, proinflammatory cytokin
转录因子Nrf2与期间是保护缺血和肾毒性急性肾损伤的作用。
氧化应激是参与急性肾损伤，由于脑缺血再灌注和化疗引起的肾毒性。探讨其基本机制的作用，我们研究核因子-红2 - p45相关因子2 （ Nrf2与） ，一个氧化还原敏感的转录因子表达的调节几个抗氧化剂和细胞保护基因。我们的反应比较Nrf2与敲除小鼠和野生型窝在建立小鼠模型的缺血再灌注损伤和顺铂所致肾毒性。几个Nrf2与调节基因编码抗氧化酶/蛋白均显着上调的肾脏野生型但不Nrf2与敲除小鼠肾缺血。肾功能，组织学，血管通透性和生存分别显着恶化的Nrf2与基因敲除小鼠。此外，促炎性细胞因子和趋化因子的表达有增加的趋势在缺血后的淘汰赛相比，野生型小鼠。治疗基因敲除小鼠的抗氧化剂N -乙酰半胱氨酸或谷胱甘肽改善肾功能。人的基因敲除小鼠更容易顺铂所致肾毒性，这是减弱的N -乙酰半胱氨酸预处理。我们的研究表明， Nrf2与缺陷增强敏感性和对缺血性急性肾损伤肾，并确定这一转录因子作为一个潜在的治疗靶点在这些injuries.Kidney推进国际在线出版物， 2009年5月13号;土井： 10.1038/ki.2009.157 。