[1]彭侃夫,赵洪雯,余荣杰,等.晚期氧化蛋白产物诱导血管平滑肌细胞表达MCP-1及其信号转导通路的研究[J].第三军医大学学报,2008,30(02):101-103.
 PENG Kan-fu,ZHAO Hong-wen,YU Rong-jie,et al.Signal transduction of advanced oxidation protein products induced MCP-1 expressions in vascular smooth muscle cells[J].J Third Mil Med Univ,2008,30(02):101-103.
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晚期氧化蛋白产物诱导血管平滑肌细胞表达MCP-1及其信号转导通路的研究(/HTML )
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
30卷
期数:
2008年第02期
页码:
101-103
栏目:
专题报道
出版日期:
2008-01-30

文章信息/Info

Title:
Signal transduction of advanced oxidation protein products induced MCP-1 expressions in vascular smooth muscle cells
作者:
彭侃夫赵洪雯余荣杰孙岩王军霞吴亿吴雄飞
第三军医大学西南医院肾科
Author(s):
PENG Kan-fu ZHAO Hong-wen YU Rong-jie SUN Yan WANG Jun-xia WU Yi WU Xiong-fei
Department of Kidney, Southwest Hospital, Third Military Medical University
关键词:
晚期氧化蛋白产物单核细胞趋化蛋白-1有丝分裂素激活蛋白激酶类鼠血管平滑肌细胞动脉粥样硬化
Keywords:
advanced oxidation protein products p38 mitogen-activated protein kinase monocyte chemotactic protein-1 vascular smooth muscle cells atherosclerosis
分类号:
R322.12;R341;R394.3
文献标志码:
A
摘要:
目的 研究p38有丝分裂素激活蛋白激酶(p38 mitogen-activated protein kinase, MAPK)在晚期氧化蛋白产物(advanced oxidation protein products, AOPP) 诱导的鼠血管平滑肌细胞单核细胞趋化蛋白-1表达中的作用。  方法 使用200和400 μmol/L AOPP分别以不同时间刺激培养的鼠血管平滑肌细-胞,在阻断实验中加入特异性p38MAPK阻断剂SB203580阻断p38MAPK信号转导通路。采用免疫印迹法(Western blot)检测细胞中MCP-1和磷酸化p38MAPK的表达情况。  结果 用特异性p38MAPK阻断剂SB203580预处理后,400 μmol/L AOPP刺激4 h的鼠血管平滑肌细胞MCP-1表达(平均灰度值)从42.00±0.95降至9.35±1.35受到显著抑制(P<0.01)。  结论 ①p38MAPK信号转导途径参与了AOPP诱导的鼠血管平滑肌细胞MCP-1的表达。②晚期氧化蛋白产物促进平滑肌细胞MCP-1 mRNA和蛋白表达可能是其致动脉粥样硬化机制之一。
Abstract:
Objective To investigate the role of p38MAPK signaling pathway in advanced oxidation protein products (AOPP) induced expressions of monocyte chemotactic protein-1 (MCP-1) in vascular smooth muscle cells (VSMCs).   Methods Vascular smooth muscle cells (VSMCs) were cultured and then co-incubated with AOPP (200, 400 μmol/L) for different time with or without the pretreatment of specific p38MAPK inhibitor SB203580. Western blot was used to detect the expression of phosphorylated p38MAPK.   Results The expression of phosphorylated p38MAPK was increased after AOPP treatment and reached the highest level 4 h after stimulation, then decreased. The expression of MCP-1 was down-regulated with the pretreatment of SB203580 as compared with that in the AOPP group (P<0.01).   Conclusion AOPP stimulates MCP-1 expression in VSMCs and contributes to the formation of atherosclerosis through this proinflammatory effect that is mediated at least in part through the activation of p38MAPK signaling pathway.

参考文献/References:

彭侃夫,赵洪雯,余荣杰,等. 晚期氧化蛋白产物诱导血管平滑肌细胞表达MCP-1及其信号转导通路的研究[J].第三军医大学学报,2008,30(2):101-103.

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更新日期/Last Update: 2008-04-29