论文部分内容阅读
目的探讨芍药苷对过氧化氢(H2O2)诱导人脐静脉血管内皮细胞(HUVEC)损伤的保护作用。方法体外培养HUVEC,以200μmol/L H2O2诱导人脐静脉血管内皮细胞损伤建立模型,同时以100、200、400μmol/L的芍药苷分别干预,显微镜下观察细胞形态,用噻唑蓝(MTT)法检测HUVEC活力,微板法检测上清液中乳酸脱氢酶(LDH)的活性及一氧化氮(NO)的含量,酶联免疫吸附法(ELISA)法检测内皮素-1(ET-1)、组织型纤溶酶原激活物(t PA)、纤溶酶原激活物抑制因子(PAI-1)的含量。结果与模型组比较,芍药苷中、高剂量组细胞活力显著升高,LDH活性显著减低、ET-1和PAI-1含量显著减少,NO和t PA显著升高(P<0.05或P<0.01)。结论芍药苷对H2O2诱导的HUVEC损伤具有明显的保护作用。
Objective To investigate the protective effect of paeoniflorin on hydrogen peroxide (H2O2) -induced injury of human umbilical vein endothelial cells (HUVECs). Methods HUVECs were cultured in vitro and induced with 200μmol / L H2O2 to induce the injury of human umbilical vein endothelial cells. Meanwhile, 100,200 and 400μmol / L of paeoniflorin were used respectively to observe the cell morphological changes. MTT assay HUVEC activity and lactate dehydrogenase (LDH) activity and nitric oxide (NO) contents in the supernatant were detected by microplate method. Endothelin-1 (ET-1) was detected by enzyme-linked immunosorbent assay (ELISA) Tissue plasminogen activator (t PA), plasminogen activator inhibitor (PAI-1) content. Results Compared with the model group, the cell viability of paeoniflorin group was significantly increased, the activity of LDH was significantly decreased, the levels of ET-1 and PAI-1 were significantly decreased, NO and t PA were significantly increased (P <0.05 or P <0.01) ). Conclusion Paeoniflorin has obvious protective effect on HUVEC induced by H2O2.