尾加压素Ⅱ在糖基化终产物诱导的肾小管上皮细胞细胞外基质合成中的作用  

Role of UrotensinⅡin advanced glycation end products-induced extracellular matrix synthesis in NRK-52E cells

作　　者：田琳[1] 贾影[1] 王果元[1] 戚基萍[1] 

机构地区：[1]哈尔滨医科大学附属第一医院病理科,黑龙江哈尔滨150001

出　　处：《哈尔滨医科大学学报》2015年第6期480-485,共6页Journal of Harbin Medical University

基　　金：黑龙江省教育厅科学技术研究课题(12541346)

摘　　要：目的研究尾加压素Ⅱ(urotensinⅡ,UⅡ)在糖基化终产物诱导的肾小管上皮细胞细胞外基质合成中的作用。方法应用体外培养大鼠近端肾小管上皮细胞(NRK-52E),采用ELISA、RT-PCR等方法,检测糖基化终产物(advanced glycation end products,AGEs)作用下,UⅡ及细胞外基质成分纤连蛋白(fibronectin,FN),四型胶原(typeⅣcollagen,ColⅣ)表达情况;同时检测UⅡ作用下,转化生长因子β1(transforming growth factor,TGF-β1)、FN及ColⅣ表达情况。结果 AGEs呈剂量和时间依赖性上调NRK-52E细胞UⅡ、FN及ColⅣmRNA表达及FN、ColⅣ蛋白分泌;UⅡ促进NRK-52E细胞TGF-β1、FN及ColⅣmRNA表达及蛋白分泌,UⅡ受体抑制剂urantide明显抑制这种效应,TGF-β1中和抗体部分抑制FN及ColⅣ蛋白分泌。结论 AGEs诱导NRK-52E细胞UⅡ表达增加,UⅡ可能是一个引起肾小管损伤和纤维化形成的新的重要致病因子。Objective To evaluate the role of urotensin Ⅱ （ UⅡ ） in extracellular matrix syn- thesis and secretion in advanced glycation end product （AGE）-stimulated NRK-52E cells. Methods NRK-52E cells were cultured in vitro under standard conditions. The contents of transforming growth factor （TGF） -β1, fibronectin（FN） and type 1Vcollagen（ CoIⅣ ） were de- termined with ELISA after stimulation by AGE-BSA and BSA, respectively. UⅡ ,TGF-β1, FN and ColIVmRNA expression were assessed by RT-PCR. Results AGEs stimulated mRNA expression of UⅡ , FN and CollV in NRK-52E cells in a dose- and time-dependent manner. In addition, UⅡ promoted TGF-β1, FN and Col lV mRNA expression and protein secretion in NRK-52E cells. Conclusion AGEs stimulate UⅡ expression in NRK-52E cells, and UⅡ may be a new important pathogenic factor in the formation of renal tubular injury and fibrosis.

关 键 词：尾加压素Ⅱ 糖基化终产物 糖尿病 

分 类 号：R587.2[医药卫生—内分泌]