Signal transduction of advanced oxidation protein products induced MCP-1 expressions in vascular smooth muscle cells

彭侃夫; 赵洪雯; 余荣杰; 孙岩; 王军霞; 吴亿; 吴雄飞

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Signal transduction of advanced oxidation protein products induced MCP-1 expressions in vascular smooth muscle cells

更新时间：2026-01-09

- Signal transduction of advanced oxidation protein products induced MCP-1 expressions in vascular smooth muscle cells
- Journal of Army Medical University Vol. 30, Issue 2, Pages: 101-103(2008)
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  CLC： R322.12;R341;R394.3
- Published：2008
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彭侃夫,赵洪雯,余荣杰,孙岩,王军霞,吴亿,吴雄飞.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].陆军军医大学学报(原第三军医大学学报),2008,30(02):101-103.

　PENG Kan-fu,ZHAO Hong-wen,YU Rong-jie,SUN Yan,WANG Jun-xia,WU Yi,WU Xiong-fei.Signal transduction of advanced oxidation protein products induced MCP-1 expressions in vascular smooth muscle cells[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(02):101-103.
彭侃夫,赵洪雯,余荣杰,孙岩,王军霞,吴亿,吴雄飞.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].陆军军医大学学报(原第三军医大学学报),2008,30(02):101-103. DOI：

　PENG Kan-fu,ZHAO Hong-wen,YU Rong-jie,SUN Yan,WANG Jun-xia,WU Yi,WU Xiong-fei.Signal transduction of advanced oxidation protein products induced MCP-1 expressions in vascular smooth muscle cells[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(02):101-103. DOI：

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(P0.01)。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 (P0.01). 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.

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Center of Nutrition and Food Safety, Chongqing Center of Medical Nutrition, Chongqing Key Laboratory of Nutrition and Food Safety, Faculty of Military Preventive Medicine, Army Medical University (Third Military Medical University)

Department of Vascular Surgery, the First Affiliated Hospital of Sun Yat-sen University

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