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作 者:刘爱军[1] 王栋[1] 朱耀斌[2] 凌锋[1] 李晓峰[1] 史强[3] 刘迎龙[2]
机构地区:[1]北京协和医学院中国医学科学院阜外心血管病医院小儿心脏外科,北京市100037 [2]首都医科大学附属北京安贞医院小儿心脏外科,北京市100029 [3]北京协和医学院中国医学科学院阜外心血管病医院卫生部心血管疾病再生医学重点实验室,北京市100037
出 处:《中华实用诊断与治疗杂志》2011年第1期7-10,共4页Journal of Chinese Practical Diagnosis and Therapy
基 金:国家自然科学基金项目(30972958)
摘 要:目的:探讨法舒地尔对血小板源性生长因子(platelet-derived growth factor,PDGF)诱导的人肺动脉平滑肌细胞(human pulmonary artery smooth muscle cell,HPASMC)增殖的抑制作用及机制。方法:以体外培养的HPASMC为研究对象,PDGF-BB诱导增殖,法舒地尔进行预处理,MTT法检测细胞增殖;流式细胞仪检测细胞周期;Western blot检测增殖细胞核抗原(proliferating cell nuclear antigen,PCNA)和p27kip1蛋白的表达。结果:细胞培养24 h后与空白组比较,PDGF组HPASMC细胞增殖比例,S期细胞比例和PCNA蛋白表达明显增加,p27kip1蛋白表达则明显降低;用法舒地尔预处理后,与PDGF组比较,细胞增殖比例,S期细胞比例和PCNA蛋白表达明显下降,p27kip1蛋白表达则明显增加。结论:法舒地尔可通过上调p27kip1蛋白表达来抑制PDGF诱导的HPASMC增殖和细胞周期进程。Objective To investigate the inhibiting effect of Fasudil on platelet-derived growth factor-induced human pulmonary artery smooth muscle cell proliferation and its mechanism.Methods Human pulmonary artery smooth muscle cells were cultured with the stimulation of platelet-derived growth factor-BB,and Fasudil in different concentrations was added before the addition of mitogen.Cell number and cell viability were determined with a hemocytometer and MTT assay respectively.The expressions of PCNA and p27kip1 protein were measured with Western blot analysis.Results Compared with control group,platelet-derived growth factor markedly induced human pulmonary artery smooth muscle cell proliferation,increased the percentage of cells in S phase and PCNA expression,but deceased p27kip1 expression.Pretreatment with Fasudil,however,significantly reversed the above effect induced by platelet-derived growth factor.Conclusion Fasudil can effectively inhibit the platelet-derived growth factor-induced human pulmonary artery smooth muscle cell proliferation and cell-cycle progression by up-regulating p27kip1.
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