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作 者:陈红霞[1,2] 谢薇[1] 魏文宁[1] 夏凌辉[1]
机构地区:[1]华中科技大学同济医学院附属协和医院血液内科,武汉430022 [2]咸宁学院基础医学院机能系,湖北咸宁437100
出 处:《临床血液学杂志》2009年第6期603-605,共3页Journal of Clinical Hematology
摘 要:目的:研究白消安(BU)对人脐静脉内皮细胞(HUVEC)一氧化氮(NO)合成及转化生长因子-β1(TGF-β1)表达的干预,并进一步探讨人参皂苷Rb1对此干预作用的影响。方法:体外培养HUVEC,以硝酸还原酶法检测各组细胞培养上清液中NO的含量,ELISA方法检测上清液TGF-β1蛋白水平,实时荧光定量PCR(Real Time-PCR)法检测HUVEC中内皮源性一氧化氮合酶(eNOS)mRNA表达。结果:BU明显抑制HUVEC合成NO及eNOSmRNA表达,而刺激TGF-β1的表达;预先用人参皂苷Rb1干预再加BU作用,发现人参皂苷Rb1可以拮抗BU对HUVEC的这种影响,提高eNOSmRNA表达及NO合成,而降低TGF-β1的表达。结论:BU可抑制HUVEC合成NO而增强TGF-β1表达,人参皂苷Rb1可拮抗此作用,人参皂苷Rb1可能籍此机制保护血管内皮细胞免受化疗药物损伤。Objective:To investigate the effects of ginsenoside Rb1 on busulfan(BU)-induced variation of nitrogen oxide(NO) synthesis and TGF-β1 expression in human umbilical vein endothelial cells(HUVECs).Method:HUVECs were cultivated in vitro.NO level in cell supernatant was tested by nitrate reductase assay.Protein level of TGF-β1 was tested by ELISA.Endothelial endothelial nitric oxide synthase(eNOS) mRNA expression was detected by real-time PCR.Result:Level of NO and expression of eNOS mRNA in HUVEC were significantly inhibited by BU,while the protein level of TGF-β1 was enhanced by BU.Ginsenoside Rb1 reversed these effects of BU in HUVEC,thus resulted in increased synthesis of NO and decreased expression of TGF-β1.Conclusion:BU could inhibit synthesis of NO and TGF-β1 in HUVEC,while ginsenoside Rb1 could reverse these effects.Ginsenoside Rb1 might protect human vascular endothelium from chemotherapeutic reagent-induced damage through this mechanism.
关 键 词:人参皂苷RB1 内皮源性一氧化氮合酶 一氧化氮
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