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dc.contributor.advisor杨云青
dc.contributor.author王光辉
dc.date.accessioned2017-06-20T08:37:22Z
dc.date.available2017-06-20T08:37:22Z
dc.date.issued2017-03-23
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/133789
dc.description.abstract背景醛糖还原酶(Aldosereductase,AR),作为山梨醇代谢通路(thepolyolpathway,PP)的限速酶,它的异常激活是导致糖尿病并发症的危险因素。先前的动物实验表明AR的抑制剂唑泊司他(zopolrestat)能显著预防糖尿病的并发症,而肾素-血管紧张素系统(therenin-angiotensinsystem/angiotensinII,RAS/AngII)控制水盐和血压平衡。但是,AR/PP与RAS/AngII之间是否存在相互作用并不清楚。在本论文中,我们进行了一系列的体内和体外实验研究,旨在揭示AR/PP与RAS/AngII相互作用的分子机制。 方法和结果我们发现...
dc.description.abstractBackground Aldose reductase (AR), the first and the rate-limiting enzyme of the polyol pathway (PP), is involved in diabetic complications. The use of AR inhibitors (ARI), zopolrestat, in preventing diabetic changes in animals strongly suggests that AR may play critical roles in the development of other diabetic complications. The renin-angiotensin system/angiotensin II (RAS/AngII) signaling...
dc.language.isozh_CN
dc.relation.urihttp://210.34.4.28/opac/openlink.php?strText=55213&doctype=ALL&strSearchType=callno
dc.source.urihttp://210.34.4.13:8080/lunwen/detail.asp?serial=54951
dc.subject高血压
dc.subject全糖还原酶
dc.subject血管紧张素
dc.subjecthypertension
dc.subjectaldose reductase
dc.subjectangiotensin
dc.title醛糖还原酶的遗传缺失显著减缓了C57BL/6小鼠AngII诱导的高血压病变进程
dc.title.alternativeAldose Reductase Defeciency Significantly Ameliorates Development of AngII-induced Hypertension in C57BL/6 mice
dc.typethesis
dc.date.replied2016-05-14
dc.description.note学位:理学博士
dc.description.note院系专业:生命科学学院_细胞生物学
dc.description.note学号:21620120153801


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