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作 者:杜航航 吴治红 陶家荣 赵四俊 马帅志 彭湘萍[2] DU Hanghang;WU Zhihong;TAO Jiarong(Clinical Medicine of Grade 16,Medical College of Jishou University,Jishou City, Hu’nan Province 416000)
机构地区:[1]吉首大学医学院临床医学系,湖南省吉首市416000 [2]吉首大学医学院生理教研室,湖南省吉首市416000
出 处:《医学理论与实践》2020年第10期1553-1555,1564,共4页The Journal of Medical Theory and Practice
基 金:吉首大学校级科研项目资助(Jdx1828);吉首大学医学类大学生创新项目资助(201810);湖南省教育厅课题资助(12C0283);湖南省卫生厅课题资助(B2012-070)。
摘 要:目的:探讨沉默信息调控因子(SIRT1)在N-甲基-D-天冬氨酸(NMDA)诱导下对肺泡上皮细胞损伤的保护作用。方法:将培养的小鼠肺上皮细胞MLE-12分为4组:Con组、NMDA组、NMDA+RSV组、RSV组。RSV为细胞SIRT1激动剂。处理24h后,CCK-8和LDH实验检测细胞活力和细胞毒性;试剂盒检测细胞培养液炎性因子TNF-α、IL-6水平;Western Blot检测细胞SIRT1表达水平。结果:与Con组相比,NMDA组细胞活力下降,培养液LDH和炎性因子水平增高,SIRT1蛋白表达降低(P<0.05)。与NMDA组相比,RSV干预使细胞活力增加,培养液LDH和炎性因子水平明显较低且SIRT1蛋白表达量增加(P<0.05)。结论:在NMDA诱导肺上皮细胞损伤中,激活SIRT1可以减轻NMDA诱导的炎性反应,具有细胞保护作用。Objective:To investigate the protective effect of SIRT1 on alveolar epithelial cell injury induced by NMDA.Methods:MLE-12 cells were divided into four groups:Con group,NMDA group,NMDA+RSV group and RSV group.RSV is a cell SIRT1 agonist.After 24 hours treatment,the cell viability and cytotoxicity were detected by CCK-8 and LDH experiments;the levels of TNF-αand IL-6 in the cell culture medium were detected by kit;the expression level of SIRT1 was detected by Western blot.Results:Compared with the Con group,the cell viability of NMDA group decreased,LDH and inflammatory factors in culture medium increased,and SIRT1 protein expression decreased(P<0.05).Compared with NMDA group,RSV intervention increased cell viability,significantly reduced LDH and inflammatory factors in culture medium,and increased SIRT1 protein expression(P<0.05).Conclusion:In NMDA induced lung epithelial cell injury,activation of SIRT1 can reduce the inflammatory response induced by NMDA,and has a cytoprotective effect.
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