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出 处:《湘南学院学报(医学版)》2016年第3期6-10,共5页Journal of Xiangnan University(Medical Sciences)
基 金:延安市科技惠民项目(2014HM-05)
摘 要:目的研究黄芩素对氧化性低密度脂蛋白所致内皮细胞损伤的保护作用,为临床研究提供参考。方法选用3种不同浓度(50μg/ml、100μg/ml和200μg/ml)ox-LDL分别处理人脐静脉内皮细胞(HUVEC)12 h、24 h和48h,筛选ox-LDL诱导内皮细胞损伤的最佳浓度和时间。HUVEC经不同浓度黄芩素(1μM、10μM和100μM)预处理1 h后,再加入终浓度100μg/ml的ox-LDL处理24 h,运用MTT比色法检测细胞活力,用NO检测试剂盒测定细胞上清液中NO浓度,用乳酸脱氢酶(LDH)检测试剂盒测定细胞上清中LDH浓度。结果 100μg/ml ox-LDL处理HUVEC 24 h时抑制细胞活力作用最明显,用于后续实验。MTT实验结果显示,与对照组比较,ox-LDL组细胞活力显著降低(P<0.05);与ox-LDL组比较,黄芩素组细胞活力显著增强(P<0.05)。NO浓度测定结果显示,与对照组比较,ox-LDL组细胞上清液中NO浓度显著降低,加入不同浓度的黄芩素可缓解ox-LDL抑制HUVEC释放NO的作用(P<0.05)。LDH浓度测定结果显示,与对照组比较,ox-LDL组细胞上清液中LDH浓度显著升高,加入不同浓度黄芩素可缓解ox-LDL促进HUVEC释放LDH的作用(P<0.05)。结论黄芩素对氧化性低密度脂蛋白所致内皮细胞损伤具有保护作用。Objective To study the protective effects of Baicalein on endothelial cell injury induced by oxidized low density lipoprotein,providing reference for clinical research. Methods Three different concentrations of ox- LDL including 50 μg / m L,100 μg / m L and 200 μg / m L were used to induce the human umbilical vascular endothelial cell( HUVEC) injury for three time points( 12 h,24 h and 48 h) respectively.The HUVEC were pretreated with three different concentrations of Baicalein including 1 μM,10 μM and 100μM for 1h,and then treated with ox- LDL( 100 μg /m L) for 24 h. MTT colorimetric method was used to measure the cell viability,the concentration of NO in cell media were measured by NO Assay Kits and the concentration of lactate dehydrogenase( LDH) in cell media were measured by LDH Assay Kits. Results100 μg / m L ox- LDL treated HUVEC for 24 h revealed the best efficiency to inhibit the cell viability,which was used for following study. The results of MTT experiment showed the cell viability in ox- LDL group decreased significantly compared with the control group( P〈0. 05),and the cell viability in Baicalein group increased significantly compared with ox- LDL group; Determination of the NO concentration indicated that the NO concentration of LDH in cell media in ox- LDL group decreased significantly with different concentrations of Baicalein relieving the inhibition of the release of No of HUVEC compared with the control group( P〈0. 05). The determination of LDH concentration discovered that the LDH concentration in cell media in ox- LDL group increased significantly with different concentrations of Baicalein relieving the inhibition of the release of No of HUVEC compared with the control group( P〈0. 05). Conclusion Baicalein exhibits protective effects on oxidized low density lipoprotein- induced endothelial cell injury.
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