论文部分内容阅读
目的 :研究二氢杨梅素(DMY)对过氧化氢(H2O2)诱导的人脐静脉内皮细胞(HUVECs)损伤的影响并探讨其作用机制。方法:用不同浓度DMY(5μg·mL-1,20μg·mL-1,80μg·mL-1)预处理保护HUVECs12 h,再用0.5 mmol·L-1 H2O2干预12 h,用MTT法检测细胞活力;用Hoechst33258进行细胞核染色;并取上清液检测超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量;用流式细胞仪分别测活性氧(ROS)和细胞内钙离子含量。结果:DMY能明显提高H2O2(0.5 mmol·L-1)损伤后HUVECs存活率(P<0.05),增加上清液SOD活性,降低MDA含量,减少细胞内ROS表达,下调细胞内钙离子浓度,其中DMY 5μg·mL-1时效果最明显。结论:DMY对H2O2诱导内皮细胞损伤具有保护作用,其机制与清除细胞内ROS,抑制细胞内钙离子介导的细胞凋亡相关,浓度以DMY 5μg·mL-1时效果最明显。
Objective: To investigate the effect of dihydromyricetin (DMY) on hydrogen peroxide (H2O2) -induced injury of human umbilical vein endothelial cells (HUVECs) and to explore its mechanism. Methods: HUVECs were pretreated with different concentrations of DMY (5μg · mL-1, 20μg · mL-1 and 80μg · mL-1) for 12 h, and then treated with 0.5 mmol·L-1 H2O2 for 12 h. The cell viability The nuclei were stained with Hoechst33258. The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were detected by supernatant. The contents of reactive oxygen species (ROS) and intracellular calcium were determined by flow cytometry. Results: DMY significantly increased the survival rate of HUVECs after 0.5 mmol·L-1 H2O2 injury (P <0.05), increased the activity of superoxide dismutase (SOD), decreased the content of MDA, decreased the intracellular ROS expression, down-regulated the intracellular calcium concentration, The effect of DMY 5μg · mL-1 was the most obvious. CONCLUSION: DMY has a protective effect on endothelial cell injury induced by H2O2. Its mechanism is related to the elimination of intracellular ROS and the inhibition of intracellular calcium-mediated apoptosis. The effect of DMY at 5μg · mL-1 is the most obvious.