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作 者:吴亮亮 陈乐蓉[1] 钟福初[1] 彭建萍[1] Wu Liangliang;Chen Lerong;Zhong Fuchu;Peng Jianping(Jiangxi Chest Hospital,Nanchang Jiangxi 330006,China)
出 处:《生命科学仪器》2024年第6期1-4,共4页Life Science Instruments
基 金:江西省自然科学基金项目(S2020ZRMSB0952),项目名称:miR-133b-5p基于EGFR/MAPK信号通路负向调控PM2.5致气道黏液高分泌的机制研究
摘 要:目的研究miR-133b-5p通过EGFR/MAPK信号通路对PM2.5引起的大鼠肺组织炎症损伤的影响。方法将48只雄性Wistar大鼠分为对照组和三个PM2.5剂量组(低、中、高),每组12只。采用气管滴注法进行PM2.5染毒。检测各组MUC5AC、TNF-α、IL-1表达水平;用qRT-PCR检测miR-133b-5p、EGFR、MUC5AC表达水平;用免疫组化法检测肺组织EGFR、MUC5AC、Caludin1蛋白表达水平;用WesternBlotting检测气道上皮EGFR、MUC5AC、Caludin1蛋白表达水平。结果与对照组相比,PM2.5各剂量组血清中MUC5AC、TNF-α、IL-1水平均显著升高(P<0.05);肺组织中miR-133b-5p、EGFR、MUC5AC表达水平均升高(P<0.05);肺组织中MUC5AC、EGFR、MAPK蛋白表达水平也呈剂量依赖性上升(P<0.05)。结论PM2.5染毒可导致大鼠肺组织中miR-133b-5p的表达水平升高,同时伴随EGFR、MAPK信号通路的激活及MUC5AC表达水平的上升。这一发现为理解PM2.5致肺损伤的分子机制提供了新的思路。Objective:To investigate the effect of miR-133b-5p on PM2.5-induced inflammatory lung injury in rats through the EGFR/MAPK signaling pathway.Methods:48 male Wistar rats were divided into control group and three groups(low、medium and high)with 12 rats in each group.PM2.5 was poisoned by tracheal instillation.The expression levels of MUC5AC、TNF-αand IL-1 in each group were detected.The expression levels of miR-133b-5p、EGFR and MUC5AC were detected by qRT-PCR.The expression levels of EGFR、MUC5AC and Caludin1 protein in lung tissue were detected by immunohistochemistry.The expression levels of EGFR、MUC5AC and Caludin1 in airway epithelium were detected by WesternBlotting.Results:Compared with the control group,the serum levels of MUC5AC、TNF-αand IL-1 in each dose group of PM2.5 were significantly increased(P<0.05);The expression levels of miR-133b-5p、EGFR and MUC5AC in lung tissue all increased(P<0.05);The expression levels of MUC5AC、EGFR and MAPK in lung tissue also increased in a dose-dependent manner(P<0.05).Conclusion:PM2.5 exposure can increase the expression level of miR-133b-5p in lung tissue of rats,accompanied by the activation of EGFR and MAPK signaling pathways and the increase of MUC5AC expression level.This discovery provides a new idea for understanding the molecular mechanism of lung injury caused by PM2.5.
关 键 词:PM2.5 miR-133b-5p EGFR/MAPK MUC5AC
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