阿托伐他汀对大鼠肾缺血再灌注损伤中tlr4的影响-肾脏内科学专业论文.docxVIP

6. Compared with the sham group, the expression of NF-κBp65 protein began to upregulate, peaked at 24 hour (P＜0.01) and it mainly expressed in cytoplasm or nucleus of renal tubule cells, but those was decreased in A group (P＜0.05).Conclusion:IRI model was established by bilateral clipping of renal arteries for 45min and reperfusion. Histopathological changes of renal tissue displayed renal tubular injury.The expression of TLR4, NF-κBp65 and IL-6 protein was gradually upregulated after renal IRI, which indicated TLR4 signal pathway activated NF-κBp65 that induces inflammatory reaction .Atorvastatin pretreatment can significantly reduce the pathological extent of renal tubular injury and the level of Scr and downregulation the expression levels of TLR4 , NF-κBp65 and IL-6, whose mechanism may be involved in the inhibition of TLR4 expression. Meanwhile cholesterol was not change obviously. These imply that atorvastatin can protect renal in independence of reducing the serum cholesterol level.KEYWORDSRenalischemiareperfusionAtorvastatinTLR4 NF-κBp65IL-6英文缩写词表英文缩写英文全称中文全称CRPC reactive proteinC 反应蛋白IL-1interleukin-1白介素 1IL-1Rinterleukin-1 receptor白介素 1 受体IL-6interleukin-6白介素 6IRIischemia-reperfusion injury缺血再灌注损伤MAPKmitogen-activated protein kinases丝裂原活化蛋白激酶MyD88myeloiddifferentiationprimary response protein 88髓样分化初级反应蛋白 88NF-κBp65nuclear factor kappa Bp65细胞核因子 κBp65Scrserum creatinine血肌酐secsecond秒TGF-βtransforming growth factor-β转化生长因子-βTIRToll/IL-1receptorhomologous domainToll/IL-1R 同源区TLRstoll-like receptorsToll 样受体TLR4toll-like receptor 4Toll 样受体 4TNF- αtumor necrosis factor肿瘤坏死因子学位论文独创性声明本人声明，所呈交的学位论文系在导师指导下本人独立完成的研究成果。文 中任何引用他人的成果，均已做出明确标注或得到许可。论文内容未包含法律意 义上已属于他人的任何形式的研究成果，也不包含本人已用于其他学位申请的论 文或成果。与我一同工作的同志对本研究所做的任何贡献均已在论文中作了明确 的说明并表示谢意。本文如违反上述声明，愿意承担以下责任和后果：1.交回学校授予的学位证书；2.学校可在相关媒体上对作者本人的行为进行通报；3.本文按照学校规定的方式，对因不当取得学位给学校造成的名誉损害， 进行公开道歉。4.本人负责因论文成果不实产生的法律纠纷。论文作者签名：日期：年月 日学位论文版权使用授权书本人完全了解山西医科大学有关保留、使用学位论文的规定，同意学校保留 或向国家有关部门或机构送交论文的复印件和电子版，允许论文被查阅和借阅； 本人授权山西医科大学可以将本学位论文