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作 者:沈雷[1] 姜杨[1] 张善强[1] 金海峰[1] 姚立杰[1] 张嵩[1] 刘丹阳[1] 李永涛[1] 王璐璐 SHEN Lei;JIANG Yang;ZHANG Shanqiang;JIN Haifeng;YAO Lijie;ZHANG Song;LIU Danyang;LI Yongtao;WANG Lulu(Qiqihar Medical University,Qiqihar 161006,China;不详)
出 处:《中国医学创新》2020年第36期26-29,共4页Medical Innovation of China
基 金:黑龙江省卫生健康委员会科研课题项目(2018470)。
摘 要:目的:验证不同浓度A549细胞上清液对人骨髓间充质干细胞(hBMSC)迁移的影响.方法:提取A549细胞上清液,以5%和25%条件培养基(CM)培养hBMSCs为5%A549-CM组、25%A549-CM组,正常培养的hBMSCs为对照组.Transwell细胞迁移实验检测各组hBMSCs划痕面积闭合率;Western blot检测各组hBMSCs中CXCL-8蛋白含量;ELISA检测各组hBMSCs的Erk、p-Erk和PI3K、p-PI3K蛋白的表达.结果:对照组、5%A549-CM组、25%A549-CM组hBMSCs细胞划痕闭合率逐渐升高,差异有统计学意义(P<0.01).与对照组比较,5%A549-CM组、25%A549-CM组hBMSCs的Erk、p-Erk和PI3K、p-PI3K蛋白表达明显增高,差异均有统计学意义(P<0.01).与对照组比较,5%A549-CM组、25%A549-CM组hBMSCs的CXCL-8蛋白表达明显增高(P<0.01).结论:A549细胞上清液能够激活hBMSCs内PI3K-Erk信号通路促进hBMSCs迁移.Objective:To verify the effect of different concentration of A549 cell supernatant on the migration of human bone marrow mesenchymal stem cells(hBMSCs).Method:The supernatant of A549 cells was extracted,and hBMSCs were cultured in 5%and 25%conditioned medium(CM)as 5%A549-CM group and 25%A549-CM group,and the normal hBMSCs were used as the control group.The scratch area closure rate of hBMSCs in each group was detected by Transwell cell migration assay.Western blot was used to detect the protein content of CXCL-8 in hBMSCs of each group.The expressions of Erk,p-Erk,PI3K and p-PI3K proteins of hBMSCs in each group were detected by ELISA.Result:Compared with the control group,the scratch closure rate of hBMSCs in the control group,5%A549-CM group and 25%A549-CM group increased gradually,the difference was statistically significant(P<0.01).Compared with the control group,Erk,p-Erk,PI3K and p-PI3K protein expressions of hBMSCs in 5%A549-CM group and 25%A549-CM group were significantly increased,the differences were statistically significant(P<0.01).Compared with the control group,the CXCL-8 protein expression of hBMSCs in 5%A549-CM group and 25%A549-CM group was significantly increased(P<0.01).Conclusion:The supernatant of A549 cells can activate the PI3K-Erk signaling pathway in hBMSCs to promote the migration of hBMSCs.
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