首页> 中文期刊> 《现代医药卫生》 >4′,5,7-三羟基异黄酮对LPS诱导的人主动脉内皮细胞ephrinB2及IL-6 mRNA表达的影响

4′,5,7-三羟基异黄酮对LPS诱导的人主动脉内皮细胞ephrinB2及IL-6 mRNA表达的影响

         

摘要

目的:探讨4′,5,7-三羟基异黄酮对脂多糖(LPS)诱导人主动脉内皮细胞(HAEC)标记物ephrinB2及炎症因子白介素-6(IL-6) mRNA表达的影响。方法体外培养HAEC,分别用浓度为0.1、1.0、10.0、100.0、1000.0μg/mL的LPS刺激HAEC 4 h,建立HAEC损伤模型。将培养的人主动脉内皮细胞分为模型组(LPS 0.1μg/mL),对照组,4′,5,7-三羟基异黄酮低(1.0μm/mL)、中(10.0μm/mL)、高(100.0μm/mL)浓度组。MTT法检测细胞的活力,Real-time PCR 法检测HAEC ephrinB2及IL-6 mRNA 表达情况。结果除10.0、100.0μg/L LPS 组外,其余各浓度组与对照组比较,均能使HAEC的活力降低,差异均有统计学意义(P<0.05);LPS能促进ephrinB2及IL-6 mRNA的表达;4′,5,7-三羟基异黄酮中、高浓度组可促进HAEC细胞活力增加,差异均有统计学意义(P<0.05);4′,5,7-三羟基异黄酮低、中浓度组可明显降低ephrinB2及IL-6 mRNA的表达,差异均有统计学意义(P<0.01)。结论适当浓度的4′,5,7-三羟基异黄酮对LPS诱导的HAEC损伤有一定的保护作用。%Objective To study the effects of 4′,5,7 trihydroxyisoflavone on mRNA expression of ephrinB2 and IL-6 in duced by LPS in human aortic endothelial cells (HAEC). Methods Human aortic endothelial cells were cultured in vitro and 0.1,1.0,10.0,100.0,1000.0μg/mL of LPS was to stimulate HAEC for 4 h. The HAEC injury model was established. Then the cultured HAEC were divided into the model group(0.1μg/mL LPS),low,middle and high 4′,5,7 trihydroxyisoflavone concentra tion groups(1.0,10.0,100.0μm/mL respectively);the cell vitality was detected by MTT assay. The mRNA expressions of ephrinB2 and IL-6 were detected by reverse transcription polymerase chain reaction (RT-PCR). Results Except for the 10.0,100.0μg/mL LPS groups,the rest other concentration groups all could reduce the vitality of HAEC compared with the control group ,the differ-ences were statistically significant(P<0.05),LPS could promote the mRNA expression of ephrinB2 and IL-6;the middle and high concentration 4′,5,7 trihydroxyisoflavone groups HAEC could promote the increase of HAEC vitality with statistical difference (P<0.05) and the low and middle concentration 4′,5,7 trihydroxyisoflavone groups could significantly reduce the mRNA expres-sion of ephrinB2 and IL-6 with statistical difference(P<0.01). Conclusion Appropriate concentration of 4′,5,7 trihdroxy-isoflavone has a certain protective effect to LPS induced HAEC injury.

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