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作 者:张宇[1] 郑为超[2] 李冬[1] 牛凯[2] ZHANG Yu;ZHENG Wei-chao;LI Dong;NIU Kai(Dept of Clinical Lab,Tongji Hospital,Tongji University,Shanghai 200065,China;Medical College,Anhui University of Science and Technology,Huainan Anhui 232001,China)
机构地区:[1]同济大学附属同济医院检验科,上海200065 [2]安徽理工大学医学院,安徽淮南232001
出 处:《中国药理学通报》2018年第10期1425-1429,共5页Chinese Pharmacological Bulletin
基 金:国家自然科学基金资助项目(No 81273777);安徽省自然科学基金资助项目(No 11040606M203);上海市卫计委青年项目(No 20154Y0033);上海市同济医院青年项目(No TJ1508)
摘 要:目的研究羟基红花黄素A(hydroxy safflower yellow A,HSYA)对退变软骨终板细胞周期的影响及相关机制。方法用10μg·L^(-1)的IL-1β诱导软骨终板细胞建立炎症退变模型,分别制备不同浓度的HSYA培养基作为干预措施,采用CCK-8法检测不同浓度HSYA对细胞增殖的影响;流式细胞仪检测HSYA对细胞周期的影响;real-time PCR检测细胞周期及凋亡相关基因p53、Bax、Bcl-xl表达;Western blot检测细胞周期相关蛋白PCNA、p53、p21表达。结果 HSYA具有促进退变软骨终板细胞增殖的作用;HSYA降低退变组细胞周期S期比例;HSYA下调退变细胞p53、Bax mRNA表达,上调Bcl-xl mRNA表达;HSYA下调退变细胞周期蛋白p53、p21表达,上调PCNA表达。结论 HSYA具有改变退变软骨终板细胞周期及抑制其凋亡的作用。To explore the cell cycle changing effects of hydroxy safflower yellow A(HSYA)on cell cycle of degenerative end-plate chondrocytes and its mechanism.Methods The endplate cartilage cell was induced by IL-1β(10μg·L-1)and established as inflammatory degeneration cell model,which was cured by HSYA in different concentrations.Then the changing of cell proliferation was analyzed in different time.Cell cycle was analyzed by using flow cytometry.The expression on cell cycle and apoptosis related genes,such as p53,Bax,Bcl-xl was detected with real-time PCR.Besides,the changing of cell cycle-related proteins PCNA,p53 and p21 was also detected by Western blot.Results The cell proliferation ability in degenerative endplate chondrocytes were promoted by HSYA with various concentrations.The ratio of S phase in degenerative group was reduced.The percentage of S phase cells decreased after treated with HSYA.Besides,HSYA down-regulated the gene expression of p53 and Bax,while it up-regulated the mRNA level of Bcl-xl.Further,HSYA decreased the cell cycle related protein expression of p53 and p21,and induced the expression level of PCNA.Conclusion HSYA could change the cell cycle and inhibit apoptosis in degenerative end-plate chondrocytes.
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