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作 者:崔川 刘佳欢 宋佳诚 梁慧婷 张义明[1] 李丽敏[1] 王家鑫[1] CUI Chuan;LIU Jia-huan;SONG Jia-cheng;LIANG Hui-ting;ZHANG Yi-ming;LI Li-min;WANG Jia-xin(College of Veterinary Medicine,Hebei Agricultural University,Baoding,Hebei.071000,China)
机构地区:[1]河北农业大学动物医学学院,河北保定071000
出 处:《中国兽医学报》2020年第2期272-277,共6页Chinese Journal of Veterinary Science
基 金:国家自然科学基金资助项目(31402174);河北省教育厅重点基金资助项目(ZD2015040);河北省自然科学基金资助项目(C2016204168)。
摘 要:为探索肥大细胞应答重组口蹄疫病毒(foot-and-mouth disease virus,FMDV)VP1-VP4(简称VP1-VP4)蛋白的信号转导途径,用重组VP1-VP4蛋白负载分别经NF-κB抑制剂获MAP激酶(MAPKs)抑制剂处理的小鼠腹腔肥大细胞(pMCs)、重组VP1-VP4负载pMCs组,以及未经处理的对照组pMCs,取1,6,24,48 h的细胞上清液,用ELISA检测细胞上清中TNF-α、IL-6和IL-10的含量。结果显示,抑制NF-κB组的IL-6和TNF-α含量在24,48 h均显著高于重组VP1-VP4负载pMCs组,而抑制MAPKs组的TNF-α、IL-6和IL-10含量在24 h以后均显著低于重组VP1-VP4负载pMCs组。结果表明,肥大细胞识别重组VP1-VP4蛋白分泌TNF-α、IL-6和IL-10受MAPKs调节,而分泌TNF-α、IL-6可能受NF-κB负调节。To study the signal transduction pathways of mast cell recognition of recombinant FMDV VP1-VP4(abbreviated as recombinant VP1-VP4) protein,mouse peritoneal mast cells(pMCs) treated by NF-κB inhibitor,pMCs treated by MAPKs inhibitor and pMCs untreated were loaded with recombinant VP1-VP4 protein.The supernatants of 1,6,24,48 h were harvest,and the level of TNF-α,IL-6 and IL-10 in the supernatants was detected by ELISA.The results showed that IL-6 and TNF-α in the group treated with NF-κB inhibitor was significantly higher than that in the group pMCs loaded with recombinant VP1-VP4 protein since 24 hours post loading,and TNF-α,IL-6 and IL-10 in the group treated with MAPKs inhibitors was significantly higher than that in the groups pMCs loaded with recombinant VP1-VP4 protein since 24 hours post loading.The results indicated that the process mast cell recognizing recombinant VP1-VP4 protein secretes TNF-α,IL-6 and IL-10 was regulated by MAPKs,and secreting IL-6 and TNF-α may negatively regulated by NF-κB.
关 键 词:口蹄疫病毒 肥大细胞 NF-ΚB MAPKS 细胞因子
分 类 号:S852.4[农业科学—基础兽医学] S852.65[农业科学—兽医学]
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