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作 者:刘圆圆 阴其玲 赫超 孟玲 LIU Yuanyuan;YIN Qiling;HE Chao;MENG Ling(Department of Respiratory Medicine,The Second Affiliated Hospital of Shandong First Medical University,Taian 271000,China;Department of Gastrointestinal Surgery,The Affiliated Taian City Central Hospital of Qingdao University,Taian 271000,China.)
机构地区:[1]山东第一医科大学第二附属医院呼吸内科,山东泰安271000 [2]青岛大学附属泰安市中心医院胃肠外科,山东泰安271000
出 处:《山东第一医科大学(山东省医学科学院)学报》2024年第5期265-268,共4页Journal of Shandong First Medical University & Shandong Academy of Medical Sciences
基 金:山东省中医药科技项目(M-2022217);泰安市科技创新发展项目(2021NS423)。
摘 要:目的研究信号转录和激活因子3(signal transduction and transcription activator3,STAT3)抑制剂WP1066对人气道上皮BEAS‑2B细胞增殖的影响及分子机制,探讨WP1066治疗支气管哮喘疾病发病的潜在机制。方法WP1066处理BEAS‑2B细胞,应用MTT法测定细胞增殖,Western Blot测定STAT3磷酸化水平及其下游靶点Cyclin D1表达水平。结果WP1066可抑制BEAS‑2B细胞的增殖,其抑制作用呈浓度依赖性,差异具有统计学意义(P<0.05);WP1066处理细胞并不会降低总的STAT3蛋白水平,但可抑制STAT3磷酸化水平,抑制下游Cyclin D1蛋白表达。结论WP1066可通过阻断STAT3信号通路,从而抑制人气道上皮细胞增殖。Objective:To investigate the effect of signal transcription and activation factor 3(STAT3)inhibitor WP1066 on the proliferation of human airway BEAS-2B cells and explore the potential molecular mechanism of WP1066 in the treatment of bronchial asthma.Methods:After pretreatment with WP1066,the proliferation of BEAS-2B cells was determined by MTT assay.The level of STAT3 phosphorylation and its downstream target Cyclin D1 were measured by Western Blot.Results:WP1066 inhibited the proliferation of BEAS-2B cells in a concentration-dependent manner.WP1066 did not reduce the total STAT3 protein level,but inhibited the phosphorylation of STAT3 and down-regulated the expression of Cyclin D1 protein.Conclusion:WP1066 can inhibit the proliferation of human airway epithelial cells by blocking the STAT3 signaling pathway.
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