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ID:34987998
大小:2.06 MB
页数:53页
时间:2019-03-15
《丁基苯酞对1型糖尿病肝损伤大鼠nrf2-are信号通路的影响》由会员上传分享,免费在线阅读,更多相关内容在学术论文-天天文库。
1、授予单位代码10089学号或申请号20122204HebeiMedicalUniversity硕士学位论文科学学位丁基苯酞对1型糖尿病肝损伤大鼠Nrf2-ARE信号通路的影响研究生:韩菲导师:孙玉凤教授专业:中西医结合临床二级学院:第二医院2015年3月河北医科大学学位论文使用授权及知识产权归属承诺本学位论文在导师(或指导小组)的指导下,由本人独立完成。本学位论文研究所获得的研究成果,其知识产权归河北医科大学所有。河北医科大学有权对本学位论文进行交流、公幵和使用。凡发表与学位论文主要内容相关的论文,第一署名为单位河北医科大学,试验材料、原始数据、申报的专利等知识产权均归河北医科大学所有。否则,
2、承担相应法律责任。.�-.k�,•*、'••“.,研究生签名导jli‘…河北医科大学研究生学位论文独创性声明本论文是在导师指导下进行的研究工作及取得的研究成果,除了文中特别加以标注和致谢等内容外,文中不包含其他人已经发表或撰写的研究成果,指导教师对此进行了审定。本论文由本人独立撰写,文责自负。研究生签名:i%导师签章.•[年3月知日中文摘要目录中文摘要·············································································1英文摘要·········································
3、····································4英文缩写·············································································8研究论文丁基苯酞对1型糖尿病肝损伤大鼠Nrf2-ARE信号通路的影响前言·············································································9材料与方法······························································
4、······10结果·············································································19附图·············································································22附表·············································································28讨论···············································
5、······························29小结·············································································33参考文献·······································································33综述Nrf2:治疗肝脏疾病的一个潜在的新靶点·····························38致谢·······················································
6、····························49个人简历·············································································50中文摘要丁基苯酞对1型糖尿病肝损伤大鼠Nrf2-ARE信号通路的影响摘要糖尿病肝损伤是指糖尿病引起的肝脏组织学和功能学的异常改变,属于糖尿病的慢性并发症,多发于2型糖尿病(T2DM)。糖尿病肝损伤常有以下病理学表现:(1)肝糖原累积;(2)脂肪肝:肝细胞内出现脂滴,多为轻度脂肪变性;(3)肝硬化:糖尿病并发肝硬变发生率较低,早期肝损伤甚至轻度脂肪变性时即可见胶原纤维增生;
7、(4)非特异性细胞变性如肝细胞嗜酸性变等;(5)微血管病变、脂肪肉芽肿等改变。近年来随着对糖尿病并发症研究的不断深入,其发病机制有包括:多元醇通路活性增高、晚期糖基化终末产物生成增多、蛋白激酶C激活、己糖胺通路活性增高。Brownlee教授等学者认为,糖尿病并发症的中心机制为“氧化应激”,即高糖引起活性氧生成过多最终导致糖尿病微血管损伤。作为机体最重要的抗氧化通路,Nrf2-ARE信号通路调控编码
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