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高糖对人肾小球系膜细胞MAPK活性的影响
作者:高景燕1 李新荣1 邓红2 刘必成3 
单位:1.东南大学基础医学院,生物化学与分子生物学系,江苏南京,210009; 2.东南大学基础医学院,病理与病理生理学系,江苏南京,210009; 3.东南大学附属中大医院肾脏科,江苏南京,210009
关键词:丝裂原蛋白激酶 高糖 人肾小球系膜细胞 糖尿病肾病 
分类号:R363, R587.2
出版年·卷·期(页码):2003·22·第六期(366-368)
摘要:

目的:研究高糖对人肾小球系膜细胞丝裂原蛋白激酶(MAPK)活性的影响,探讨其在糖尿病肾病发病中的作用.方法:采用人肾小球系膜细胞进行体外培养,按培养液中葡萄糖浓度分为对照组(含11mmol*L-1葡萄糖)、高糖组(含30mmol*L-1葡萄糖)、MAPK抑制剂组(含25μmol*L-1PD98059加30mmol*L-1葡萄糖)及甘露醇组(含20mmol*L-1甘露醇),以32P标记的髓磷脂碱性蛋白为底物,用同位素示踪技术测定培养细胞的MAPK活性.结果:高糖组MAPK活性明显高于其它各组;加入MAPK抑制剂后,其活性明显降低,同时细胞的增殖受到抑制.结论:高糖可增加人肾小球系膜细胞MAPK活性,且可能与渗透压引起的应激刺激相关.

Objective   To study the effects of high glucose on activity of mitogen activated protein kinase (MAPK) in cultured human mesangial cells and to explain the mechanism of diabetic nephropathy. Methods  The human mesangial cells were incubated and divided into five groups according to the concentration of glucose in medium: normal group (11-mmol·L    -1 glucose); high glucose group (30-mmol·L    -1glucose);the MAPK special inhibitor PD98059 group (25-μmol·L    -1 PD98059+30-mmol·L    -1 glucose) and mannitol group (20-mmol·L    -1  mannitol) as osmolity control. We used the MBP marked by       32P as substance to test the activity of MAPK. Result  The activity of MAPK in the high glucose group was higher than that in the other groups.When treated with PD98059 ,the cell proliferation was inhibited. Conclusion  The activity of MAPK in human mesangial cells increases when treated with high glucose,which may be related with the stress-activation induced by osmolity.

参考文献:

[1] Tomlinson D R. Mitogen-activated protein kinases as glucose transducers for diabetic complications. 1999. doi:10.1007/s001250051439
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[5] 李田昌, 庞永正, 苏静怡. 丝裂素活化蛋白激酶活性测定, 1996(2)
[6] 李慎军, 张忠辉. 糖尿病肾病基底膜成分的改变. 国外医学(内分泌学分册)2000(3). doi:10.3760/cma.j.issn.1673-4157.2000.03.007
[7] 魏日胞, 陈香美, 李文歌. 高糖促进肾小球系膜细胞纤维连接蛋白合成的实验研究. 解放军医学杂志2002(1)
[8] JOHN H O, HOUJOO H A, MIRA Y U. Sequential effects of high glucose on mesangial cell transforming growth tactor-β1 and fibronectin synthesis. 1998. doi:10.1046/j.1523-1755.1998.00193.x 

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