去甲基雏菊叶龙胆酮对Ox-LDL诱导内皮细胞衰老的影响  

Demethylbellidifolin inhibits oxidative low-density lipoprotein induced senescence of endothelial cells

作　　者：向田[1] 解媛媛[1] 袁琼[2] 刘超[1] 刘思妤[2] 黄鹤[1] 徐康平[3] 姜德建[2] 

机构地区：[1]中南大学湘雅医学院临床医学系,2004级八年制长沙410013 [2]中南大学药学院药理学系,长沙410078 [3]中南大学药学院药物化学系,长沙410013

出　　处：《中南药学》2008年第5期513-516,共4页Central South Pharmacy

基　　金：国家自然科学基金(30700319)

摘　　要：目的研究酮化合物去甲基雏菊叶龙胆酮(DMB)对氧化型低密度脂蛋白(Ox-LDL)致内皮细胞衰老的影响。方法培养人脐静脉内皮细胞(HUVECs),Ox-LDL(100μg.mL-1)处理48 h后,检测β-半乳糖苷酶活性(染色法)和端粒酶活性(TRAP-银染法)评价细胞衰老状态;使用荧光染料H2DCF检测细胞内氧自由基生成。结果Ox-LDL(100μg.mL-1)处理48 h后,β-半乳糖苷酶染色阳性细胞数显著增加,而端粒酶活性显著降低。预先1 h给予不同浓度的DMB(1、3和10μmol.L-1)并孵育48 h可显著抑制Ox-LDL诱导的内皮细胞β-半乳糖苷酶染色阳性细胞数增加和端粒酶活性降低。Ox-LDL(100μg.mL-1)孵育HUVECs 48 h,可明显增强细胞内活性氧族(ROS)水平,其效果能被预处理DMB所逆转。结论DMB抑制Ox-LDL诱导的内皮细胞衰老,其作用可能与抑制氧化应激有关。Objective To investigate the effect of demethylbellidifolin （DMB）, a xanthone compound, on oxidative low-density lipoprotein （Ox-LDL） -induced senescence of endothelial cells, Methods Human umbilical vein endotheli al cells （HUVECs） were cultured and treated with Ox-LDL （100μg · mL^-1） for 48 h to induce senescence reflected by both senescence-associated beta-galactosidase activity and telomerase activity. The level of intracellular reactive oxygen species （ROS） was determined by H2DCF, an oxidant-sensitive fluorscent indicator. Results Treatment with Ox-LDL （100μg · mL^-1） for 48 h significantly increased heta-galactosidase-positive cell ratio and reduced telomerase activity, which could be markedly attenuated by pretreatment with DMB （1, 3 and 10μmol · L^-1 ）. Also, the elevation of intracellular ROS production elicited by Ox-LDL was significantly suppressed by pretreatment with DMB. Conclusion DMB can inhibit Ox-LDI=induced senescence of endothelial cells, and such effect of DMB may be related to inhibiting intracellular ROS production.

关 键 词：去甲基雏菊叶龙胆酮 内皮细胞 衰老 氧化应激 

分 类 号：R965[医药卫生—药理学]