| 咯利普兰通过MAPK/ERK信号通路抑制中性粒细胞的黏附 |
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| 引用本文： | 孔学礼,王亚楠,丛心宇,李佳,陈武,姜代勋.咯利普兰通过MAPK/ERK信号通路抑制中性粒细胞的黏附[J].北京农学院学报,2018,33(2):58-63. |
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| 作者姓名： | 孔学礼 王亚楠 丛心宇 李佳 陈武 姜代勋 |
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| 作者单位： | 北京农学院动物科学技术学院/兽医学(中医药)北京市重点实验室,北京,102206;北京农学院动物科学技术学院/兽医学(中医药)北京市重点实验室,北京,102206;北京农学院动物科学技术学院/兽医学(中医药)北京市重点实验室,北京,102206;北京农学院动物科学技术学院/兽医学(中医药)北京市重点实验室,北京,102206;北京农学院动物科学技术学院/兽医学(中医药)北京市重点实验室,北京,102206;北京农学院动物科学技术学院/兽医学(中医药)北京市重点实验室,北京,102206 |
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| 基金项目： | 北京市自然科学基金资助项目(6152003/6112007) |
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| 摘 要： | 【目的】研究磷酸二酯酶4(PDE4)特异性抑制剂咯利普兰抑制中性粒细胞黏附的有关分子机制,明确其抗炎的主要信号通路,为PDE4选择性中药抑制剂的药理研究提供参考。【方法】猪中性粒细胞的提取采用密度梯度离心法,中性粒细胞与猪内皮细胞的黏附采用虎红比色法,中性粒细胞黏附分LFA-1和Mac-1表达量的检测采用流式细胞技术,中性粒细胞p38MAPK、ERK等磷酸化活性检测采用western blot法。【结果】咯利普兰可显著抑制fMLP刺激的中性粒细胞和内皮细胞的黏附(P0.05),极显著抑制fMLP刺激的中性粒细胞LFA-1和Mac-1的表达(P0.01),阻断fMLP刺激的中性粒细胞ERK磷酸化活性(P0.01),而对p38MAPK磷酸化活性无显著影响。【结论】咯利普兰可抑制中性粒细胞和内皮细胞黏附,其机制与阻断中性粒细胞ERK磷酸化进而抑制LFA-1和Mac-1表达有关。
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| 关 键 词： | ERK p38MAPK 黏附分子 LFA-1 Mac-1 中性粒细胞 |
Rolipram inhibits neutrophils adhesion by MAPK and ERK signaling pathway |
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| KONG Xueli,WANG Yanan,CONG Xinyu,LI Jia,CHEN Wu,JIANG Daixun.Rolipram inhibits neutrophils adhesion by MAPK and ERK signaling pathway[J].Journal of Beijing Agricultural College,2018,33(2):58-63. |
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| Authors: | KONG Xueli WANG Yanan CONG Xinyu LI Jia CHEN Wu JIANG Daixun |
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| Abstract: | Objective]To study the molecular mechanism of rolipram,a specific inhibitor of phosphodiesterase type 4 (PDE4),on the inhibition of neutrophils adhesion,elucidate the main pathway of anti-inflammation,and provide a reference for the pharmacological study of PDE4 selective herbal inhibitors.Methods]Density gradient centrifugation was used to extract porcine neutrophils,Tiger red colorimetric method was used to detect the adhesion of neutrophils to porcine endothelial cells,the adhesion molecules,LFA-1 and Mac-1,of neutrophils were detected by flow cytometry,and the phosphorylation of p38MAPK and ERK in neutrophils was detected by Western blot.Results]Rolipram could significantly inhibit fMLP-stimulated adhesion of neutrophils and endothelial cells (P ＜ 0.05),significantly inhibit fMLP-stimulated expression of LFA-1 and Mac-1 on neutrophils (P ＜ 0.01),block fMLP-stimulated ERK phosphorylation activity in neutrophils (P ＜ 0.01),but could not show any significant effect on p38MAPK phosphorylation.Conclusion]Rolipram can inhibit the adhesion of neutrophils and endothelial cells,and its mechanism maybe relate to blocking ERK phosphorylation and inhibiting LFA-1 and Mac-1 expression of neutrophils. |
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