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ID:35152048
大小:1.73 MB
页数:44页
时间:2019-03-20
《参芍口服液对糖尿病大鼠心肌纤维化及炎性损伤的影响及机制的研究》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20122466HebeiMedicalUniversity硕士学位论文科学学位参芍口服液对糖尿病大鼠心肌纤维化及炎性损伤的影响及机制的研究研究生:吕冰导师:尚小明教授专业:内科学二级学院:唐山工人医院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、公开和使用。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
2、数据、申报的专利等知识产权均归河北医科大学所有。否则,承担相应法律责任。研究生签名导师签章: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:名?I导师签章:yois年;月州曰目录中文摘要·············································································1英文摘要···
3、··········································································4英文缩写·············································································9研究论文参芍口服液对糖尿病大鼠心肌纤维化及炎性损伤的影响及机制的研究前言·············································································1
4、0材料与方法····································································10结果·············································································17附图·············································································20附表·······························
5、··············································24讨论·············································································25结论·············································································28参考文献·························································
6、··············28综述肿瘤坏死因子-α与糖尿病并发症关系的研究现状················32致谢···················································································40个人简历·············································································41中文摘要参芍口服液对糖尿病大鼠心肌纤维化及炎性损伤的影响及机制的研究摘要目的:大量研究
7、证实糖尿病心肌病(Diabeticcardiomyopathy,DCM)出现心肌损伤是多因素的,肾素-血管紧张素-醛固酮系统(Renin-angiotensinaldosteronesystem,RAAS)及炎性因子的激活在其中发挥着重要作用。p38丝裂原活化蛋白激酶(Mitogen-activatedproteinkinase,MAPK)与心肌纤维化密切相关,并可通过调节核转录因子-κB(Nucleartranscriptionfactor-κB,NF-κB)的表达影响糖尿病心肌病的炎性损伤过程。目前研究表明血管紧张素Ⅱ(Angiot
8、ensinⅡ,AngⅡ)及其特异性1型受体——血管紧张素Ⅱ1型受体(Angiotensintype1receptor,AT1R)介导RAAS,当AngⅡ激活心肌细胞膜上的AT1R后可上调p38MAPK的表达
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