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目的观察川芎嗪(TMP)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及机制。方法通过密度梯度离心分离脐静脉血单个核细胞,利用血管内皮生长因子(VEGF)诱导纯化方法培养EPCs。CCK-8细胞计数试剂盒、流式细胞仪、激光共聚焦显微镜检测TMP对细胞氧化应激损伤的保护作用及机制探讨。结果200mg·L–1TMP抑制内皮祖细胞增殖功能;但是25mg·L-1TMP显著减少H2O2致细胞凋亡和细胞生长停滞在G0/G1期,而L-单甲基精氨酸(L-NMMA)抵消TMP的保护作用。结论TMP对氧化应激损伤诱导细胞凋亡和生长停滞具有明显的保护作用,eNOS受体拮抗剂L-NMMA能抵消TMP这种保护作用,说明TMP对EPCs抗氧化应激损伤的保护作用可能是通过eNOS途径。
Objective To investigate the protective effect and mechanism of ligustrazine (TMP) on oxidative stress injury induced by hydrogen peroxide (H2O2) in endothelial progenitor cells (EPCs). Methods Human umbilical vein blood mononuclear cells were isolated by density gradient centrifugation and purified by vascular endothelial growth factor (VEGF). CCK-8 cell counting kit, flow cytometry, confocal laser scanning microscopy TMP on cell oxidative stress injury and its mechanism of action. Results Twenty-five mg · L-1 TMP inhibited the proliferation of endothelial progenitor cells. However, 25 mg · L-1 TMP significantly reduced the apoptosis induced by H2O2 and the cell growth arrested in G0 / G1 phase. However, L-monomethyl arginine (L-NMMA) Offset TMP protection. Conclusion TMP has a significant protective effect on oxidative stress-induced apoptosis and growth arrest. The protective effects of TMP on L-NMMA receptor antagonist L-NMMA can counteract the possible protective effect of TMP on the oxidative stress-induced injury of EPCs Via the eNOS pathway.