曲美他嗪对内皮祖细胞氧化应激损伤的保护作用研究

发布时间：2018-01-02 16:03

本文关键词：曲美他嗪对内皮祖细胞氧化应激损伤的保护作用研究　出处：《中国医院药学杂志》2016年10期 　论文类型：期刊论文

【摘要】：目的:研究曲美他嗪(TMZ)对过氧化氢(H2O2)诱导的内皮祖细胞(EPCs)氧化应激损伤的保护作用。方法:采用密度梯度离心法分离人脐带血单个核细胞,使用EBM-2完全培养基诱导单个核细胞向内皮祖细胞分化,经细胞形态学变化及流式细胞术测定内皮祖细胞特异性标记物CD133、CD34和VEGFR抗原来鉴定内皮祖细胞。体外建立内皮祖细胞过氧化氢(100μmol·L~(-1))损伤模型,加入不同浓度曲美他嗪(0.1,0.5,1,5μmol·L~(-1)),观察曲美他嗪作用不同时间后(0.5,1,6,12 h)内皮祖细胞增殖、黏附、迁移、一氧化氮(NO)分泌能力的变化。结果:曲美他嗪呈剂量及时间依赖性降低过氧化氢对内皮祖细胞的氧化应激损伤,保护内皮祖细胞增殖、黏附、迁移、分泌的生物学功能。结论:曲美他嗪在氧化应激条件下对内皮祖细胞生物学功能的保护可能是其心血管保护作用的机制之一。
[Abstract]:Objective: To study the Sibutramine trimetazidine (TMZ) on hydrogen peroxide (H2O2) induced endothelial progenitor cells (EPCs) protective effect on oxidative stress injury. Methods: isolated human umbilical cord blood mononuclear cells by density gradient centrifugation using EBM-2 complete medium inward progenitor cells mononuclear cells were induced by cell morphology and flow. Cytometry determination of specific endothelial progenitor cell markers CD133, CD34 and VEGFR against the original identification of endothelial progenitor cells. In vitro endothelial progenitor cells to hydrogen peroxide (100 mol - L~ (-1)) injury model with different concentrations of trimetazidine (0.1,0.5,1,5 mol - L~ (-1)), to observe Sibutramine trimetazidine the effect of different time (0.5,1,6,12 H) proliferation, endothelial progenitor cell adhesion, migration, nitric oxide (NO) secretion ability changes. Results: QuMei trimetazidine was dose and time dependent decrease in hydrogen peroxide oxidative stress on endothelial progenitor cells, protection Conclusion: the protective effect of trimetazidine on endothelial progenitor cells under oxidative stress may be one of the mechanisms of cardiovascular protection.

【作者单位】：华中科技大学同济医学院附属武汉市中心医院综合二科;华中科技大学同济医学院附属协和医院老年科;驻马店市中心医院神经内科;德州大学西南医学中心心脏病学部心内科;
【基金】：武汉市科技局2013年国际合作项目(编号:2023030409020110)
【分类号】：R96
【正文快照】： 驻马店463000;4.德州大学西南医学中心心脏病学部心内科,美国德州77377)Protective effects of trimetazidine on endothelial progenitor cells against oxidative stress injuryinduced by H2O2血管内皮细胞的氧化应激损伤是动脉粥样硬化发生发展的重要环节[1]。内皮祖细胞(

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