p38MAPK/eNOS信号通道在胰高血糖素样肽-1抑制AGEs诱导的人脐静脉内皮细胞凋亡中的作用 |
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引用本文: | 曾海龙,黄志秋,张艺能,孙慧琳. p38MAPK/eNOS信号通道在胰高血糖素样肽-1抑制AGEs诱导的人脐静脉内皮细胞凋亡中的作用[J]. 南方医科大学学报, 2016, 36(1): 116. DOI: 10.3969/j.issn.1673-4254.2016.01.21 |
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作者姓名: | 曾海龙 黄志秋 张艺能 孙慧琳 |
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作者单位: | 1. 广东药学院附属第一医院内分泌科,广东 广州,510080;2. 广东药学院附属第一医院科教科,广东 广州,510080 |
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基金项目: | 广东省自然科学基金(S2011010002074),清远市科技计划项目(2011B011112044) |
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摘 要: | 目的探讨p38MAPK信号通道在胰高血糖素样肽-1(GLP-1)拮抗糖基化终末产物(AGEs)诱导的人脐静脉内皮细胞凋亡 的作用。方法实验组分为对照组、AGEs组、GLP-1组、AGEs+GLP-1组、AGEs+抑制剂组及AGEs+GLP-1+抑制剂组,western blot技术检测p-p38MAPK/p38MAPK、p-eNOS/eNOS蛋白表达情况,Annexin V/PI流式检测细胞凋亡率。结果与对照相比较, 单独加入AGEs或GLP-1可分别导致p-p38MAPK蛋白表达水平明显上升(P=0.001)或下降(P<0.001);与对照组相比AGEs可 显著降低p-eNOS表达水平(P=0.007),而予以GLP-1或p38MAPK抑制剂(SB203580)预处理后,受抑制的eNOS蛋白表达水平 再次显著升高(P=0.004);在AGEs 组加入SB203580 或GLP-1 预处理后,AGEs诱导的细胞凋亡率均显著下降(P<0.001,P< 0.001)。结论GLP-1至少部分通过抑制p38MAPK蛋白磷酸化,上调磷酸化eNOS蛋白的表达,对人脐静脉内皮细胞起到抗凋 亡的保护作用。
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关 键 词: | 胰高血糖素样肽-1 p38MAPK 人脐静脉内皮细胞 内皮细胞损伤 糖基化终末产物 |
Role of p38MAPK/eNOS signaling pathway in the inhibition of AGEs-induced apoptosis of human umbilical vein endothelial cells by glucagon-like peptide-1 |
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Abstract: | Objective To investigate the role of p38MAPK signaling pathway in the mechanism by which glucagon-like peptide-1 (GLP-1) inhibits endothelial cell damage induced by AGEs. Methods Human umbilical vein endothelial cells were divided into control group, AGEs group, GLP-1 group, AGEs + GLP-1 group, AGEs + inhibitor group, and AGEs + GLP-1 + inhibitor group. The expressions of p-p38MAPK/p38MAPK and p-eNOS/eNOS protein were examined by Western blotting, and the cell apoptosis rates were tested by flow cytometry. Results Compared with the control group, AGEs significantly enhanced the expression of p-p38 MAPK protein (P=0.001) while GLP-1 significantly inhibited its expression (P<0.001). AGEs significantly inhibited the expression of p-eNOS protein (P=0.007), which was enhanced by GLP-1 and p38 MAPK inhibitor (SB203580) (P=0.004). Both SB203580 and GLP-1 treatment decreased the apoptosis rate of AGEs-treated cells (P<0.001). Conclusion GLP-1 can protect human umbilical vein endothelial cells against AGEs-induced apoptosis partially by inhibiting the phosphorylation of p38MAPK protein and promoting the expression of p-eNOS protein.
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Keywords: | glucagon-like peptide-1 p38MAPK human umbilical vein endothelial cells endothelial cell apoptosis Advanced glycation endproducts |
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