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作 者:齐瑞云 孙洁[2] 朴金花[2] QI Rui-yun;SUN Jie;PIAO Jin-hua(Clinical School of Medicine, Jiamusi University, Jiamusi 154003, China;Jiamusi University Basic Medical College,Jiamusi 154007,China)
机构地区:[1]佳木斯大学临床医学院,黑龙江佳木斯154003 [2]佳木斯大学基础医学院,黑龙江佳木斯154007
出 处:《黑龙江医药科学》2019年第4期26-27,30,共3页Heilongjiang Medicine and Pharmacy
基 金:佳木斯大学校长创业基金项目,编号:XZYF2017-22;黑龙江省卫生厅科学技术研究项目,编号:2009-349
摘 要:目的:评价比较细胞复制性衰老和应激诱导的MRC-5细胞早衰过程。方法:将MRC-5人胚肺成纤维细胞分为青年对照组(24PDL)、复制性衰老组(50PDL)和H2O2诱导的早衰细胞组,对细胞形态学变化和衰老相关β-半乳糖苷酶染色(SA-β-gal)衰老指标进行综合评价。结果:对于细胞复制性衰老与MRC-5细胞早老模型,二者在衰老过程中所表现出细胞形态学及SA-β-gal染色阳性细胞率等方面的变化是一致的,且应激诱导的MRC-5细胞早衰过程中所表现出的衰老相关变化更为显著。H2O2作为体外诱导剂成功构建MRC-5细胞早老模型(通过相关细胞形态学变化及SA-β-gal染色验证),两种细胞衰老方式在其转录调控机制上有其共同之处。结论:尽管衰老机制不同,但细胞复制性衰老和应激诱导的细胞早衰过程转录调控机制相似,可能与DNA损伤加重或氧化应激水平升高有关。Objective: To evaluate and compare the process of cellular replicative senescence and stress-induced premature senescence of mrc-5 cells.Methods: mrc-5 human embryonic lung fibroblasts were divided into youth control group (24 PDL), replicative senescence group (50 PDL) and H 2O 2-induced progeria group.Morphological changes and senescence related beta galactosidase staining (SA-beta-gal) were evaluated.Results: The cell morphology and sa-bet-gal positive cell rate in the mrc-5 premature senescence model were consistent with those in the mrc-5 premature senescence model.Senescence related changes in stress-induced premature senescence of mrc-5 cells were more significant.H 2O 2 can be used as an in vitro inducer to successfully construct the mrc-5 cell premature senescence model (verified by relevant cell morphological changes and sa-bet-gal staining). The two cell senescence methods have similarities in transcriptional regulation mechanism.Conclusion: Although the mechanism of senescence is different, the transcriptional regulation mechanism of cell replicative senescence and stress-induced premature senescence is similar, which may be related to the aggravation of DNA damage or the increase of oxidative stress level.
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