摘要
目的研究氧自由基对内皮祖细胞(endothelial progenitor cells,EPCs)的损伤及槲皮素(quercetin,Que)的保护作用,并探讨可能机制。方法①分离内皮祖细胞并诱导其分化,随机分为:空白对照组;60～120μmol/L Que组;H2O2组;60～120μmol/L Que+H2O2组。②WST-1观察细胞增殖情况;③应用免疫细胞化学染色法观察p-JNK蛋白;④流式细胞术分析细胞凋亡改变。结果①低浓度的Que可以促进EPCs的增殖,而高浓度的Que则表现为抑制其增殖(P<0.05);②Que在60～120μmol/L范围内呈浓度依耐性降低H2O2诱导的EPCs凋亡率(P<0.01);③Que能抑制加入JNK激动剂后EPCs凋亡率的增加(P<0.05)。结论Que可促进H2O2诱导的EPCs的增殖,并通过阻断JNK信号通路抑制其凋亡。Que具有拮抗氧化应激条件下EPCs损伤的潜在作用。
【Objective】 To investigate the protective effects of quercetin（Que） on peroxide（H2O2）-injured endothelial progenitor cells（EPCs）,so as to illustrate its underlying mechanism.【Methods】 EPCs were isolated from human umbilical cord blood and characterized.After 7～8 days of culture,EPCs were divided into control group,Que group（60 μmol/L,90 μmol/L,120 μmol/L）,H2O2 group（500 μmol/L）,Que（60 μmol/L,90 μmol/L,120 μmol/L） ＋H2O2（500 μmol/L） group.WST-1 was used to observe cell proliferation.The expression of p-JNK was detected by immunocytochemistry.The cellular apoptosis were assessed by flow cytometry using annexin-V FITC/propidium iodide.【Results】 ① Cellular proliferation was promoted by Que（60～90 μmol/L）.② When adding Que to EPCs that induced by H2O2,the apoptosis rate was obviously decreased.③ Que could inhibit the increase of apoptotic rate of EPCs after JNK agonist was added.【Conclusion】 Que can promote the proliferation of EPCs induced by H2O2,and regulate the apoptosis by blocking the JNK pathway.Que has the effect to inhibit the damage of EPCs in oxidative stress.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2012年第10期22-28,共7页
China Journal of Modern Medicine
关键词
槲皮素
内皮祖细胞
增殖
凋亡
quercetin
endothelial progenitor cells
proliferation
apoptosis
