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作 者:赵晶[1] 徐守竹[1] 宋凡[1] 年伦 周暄宣[1] 王四旺[1]
机构地区:[1]第四军医大学药学系天然药物学教研室,陕西西安710032
出 处:《中成药》2015年第3期487-492,共6页Chinese Traditional Patent Medicine
基 金:陕西省科技统筹重大专项(2012KTCQ03-02)
摘 要:目的探讨从何首乌提取的二苯乙烯苷(TSG)对溶血卵磷脂(LPC)诱导人脐静脉血管内皮细胞(HUVECs)凋亡的影响及其可能机制。方法体外培养HUVECs,筛选溶血卵磷脂损伤内皮细胞的最适药物浓度,采用CCK-8检测细胞活力,透射电镜观察细胞形态,激光共聚焦显微镜检测和观察活性氧(ROS)水平,Western blot检测p-JNK蛋白的水平。结果 LPC能引起细胞损伤,并随质量浓度增加,细胞活力降低,其中10μg/mL LPC作用细胞后,与正常组比较细胞活力明显降低,细胞内空泡增多,线粒体肿胀,产生ROS的水平增高,p-JNK蛋白表达水平显著上调。经二苯乙烯苷预处理1 h后,二苯乙烯苷1.0μmol/L和10μmol/L组与溶血卵磷脂组比较,细胞活力增强,细胞内空泡减少,线粒体较完整,产生ROS水平降低,p-JNK蛋白表达量显著下调(P<0.05)。结论二苯乙烯苷具有降低溶血卵磷脂所致HUVECs的细胞损伤作用,其机制可能与调节ROS相关JNK通路有关。AIM To study the protective effect of 2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glucoside( TSG)extracted from Polygoni multiflori Radix on lysophosphatidylcholine( LPC)-induced HUVECs and to explore its possible mechanism.METHODS After treating HUVECs with LPC( 5 μg / m L,10 μg / m L,20 μg / m L,40μg /m L) for 24 h,the optimal concentration of LPC was chosen based on the results from MTT assay and the cell viability was measured by CCK-8 assay.Transmission electron microscope was used to study cell morphology.The level of reactive oxygen species( ROS) production in HUVECs was observed by laser scanning confocal microscope.The expression of p-JNK was detected by Western-blot.RESULTS LPC could induce endothelial cell injury.The cell viability decreased with the increase of the concentration of LPC.Compared with DMEM group,the concentration of 10 μg / m L LPC significantly decreased the cell viability,increased the cell vacuoles,caused mitochondria to swell,increased the production of ROS and significantly up-regulated the expression of p-JNK.Compared with LPC group,TSG treatment group( 1.0 μmol / L and 10.0 μmol / L) enhanced the cell viability,decreased cell vacuoles,mitochondria with complete cristae,and down-regulated the expression of p-JNK( P〈0.05).CONCLUSION TSG inhibits LPC-induced damage to HUVECs,which may be associated with regulating ROS- related JNK pathway.
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