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作 者:赵梦瑶 李思源[2] 肖志伟 蔺茹君 赵晓伟 李军[1] ZHAO Mengyao;LI Siyuan;XIAO Zhiwei;LIN Rujun;ZHAO Xiaowei;LI Jun(Department of Endocrinology and Metabolism,The First Affiliated Hospital of the Medicine College,Shihezi University,Xinjiang Shihezi 832000,China;Shihezi University School of Medicine,Xinjiang Shihezi 832000,China;69296 Troops of the Xinjiang Military Region,Xinjiang Kashi 844000,China)
机构地区:[1]石河子大学医学院第一附属医院内分泌代谢科,石河子832000 [2]石河子大学医学院,石河子830000 [3]新疆军区69296部队,喀什844000
出 处:《广州医药》2020年第1期10-13,共4页Guangzhou Medical Journal
基 金:兵团区域创新引导计划(2018BB040);兵团中青年科技创新领军人才专项(2015BC001)
摘 要:目的利用分析各种浓度环氧化酶-2(COX-2)特异度抑制剂塞来昔布对食管癌EC109细胞系的作用,进而对COX-2蛋白表达的影响及对细胞凋亡能力的作用,进一步探讨塞来昔布对食管癌细胞凋亡的作用及机制。方法使用0μmol/L、20μmol/L、60μmol/L、100μmol/L四个浓度的塞来昔布处理EC109细胞24 h,酶联免疫吸附剂测定(ELISA)法测定COX-2蛋白表达;流式细胞仪测定EC109细胞凋亡情况。结果与0μmol/L塞来昔布组比较,20μmol/L、60μmol/L、100μmol/L塞来昔布组EC109细胞内COX-2蛋白表达不断降低(1.581±0.116;1.226±0.089,0.846±0.076,0.521±0.082)(P<0.05);而细胞凋亡率逐步上升(1.700±0.557,13.400±1.735,18.766±1.301,28.100±1.997)(P<0.05)药物浓度依赖于梯度。结论塞来昔布是一种COX-2抑制剂,可能以浓度梯度的形式抑制COX-2蛋白的表达,从而促进EC109细胞的凋亡。Objective The effects of celecoxib,a specific COX-2 inhibitor at various concentrations,on EC109 cell line of esophageal cancer were analyzed,and the effect and mechanism of celecoxib on apoptosis of esophageal carcinoma cells were further studied.Methods EC109 cells were treated with celecoxib at concentrations of 0μmol/L,20μmol/L,60μmol/L and 100μmol/L for 24 h.The protein of COX-2 in EC109 cells was determined by enzyme-linked immunosorbent assay(ELISA).Assay of EC109 cell apoptosis were determined by flow cytometry.Results Compared with the 0μmol/L celecoxib group,the expression of COX-2 protein in EC109 cells of 20μmol/L,60μmol/L,100μmol/L celecoxib group gradually decreased(1.581±0.116;1.226±0.089,0.846±0.076,0.521±0.082)(P<0.05);and the apoptotic rate gradually increased(1.700±0.557;13.400±1.735,18.766±1.301,28.100±1.997)(P<0.05)in a drug concentration gradient-dependent manner.Conclusion The COX-2 inhibitor celecoxib may inhibit the expression of COX-2 protein in a concentration gradient and promote the apoptosis of esophageal cancer EC109 cells.
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