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目的:探讨二苯乙烯苷(TSG)对血管内皮细胞在溶血性磷脂酰胆碱(LPC)诱导下的保护作用及其机制。方法:体外培养人脐静脉血管内皮细胞(HUVECs),将TSG以10.0;1.0;0.1mol/L预先作用于HUVECs 1小时后,继续培养,再给予10mg/L的LPC作用于HUVECs共同孵育24小时,检测细胞的存活率、MDA、NO和ROS的变化。结果:以10mg/L浓度LPC的模型组与对照组比较结果显示,观测到细胞培养上清液中MDA含量显著性增加,而细胞培养上清液中NO含量明显降低,细胞的活性氧水平有所增加,细胞的存活率降低。实验组与模型组比较发现,以0.1μmol/L作为起效剂量,在0.1～10.0μmol/L浓度的范围内有效,并具有一定的浓度依赖关系。随着药物有效浓度的增加,细胞培养上清液中MDA含量显著性降低,NO含量显著性升高,细胞的活性氧水平则降低和细胞的存活率却显著性升高。结论:二苯乙烯苷能够通过抑制活性氧水平,增加NO的生成,增加细胞的存活,从而对LPC损伤的血管内皮细胞发挥保护作用。
AIM: To investigate the protective effect of stilbene glycoside (TSG) on vascular endothelial cells induced by hemolytic phosphatidylcholine (LPC) and its mechanism. Methods: Human umbilical vein endothelial cells (HUVECs) were cultured in vitro. The TSGs were pre-treated with HUVECs (10.0, 1.0, 0.1 mol / L) for 1 hour. The cultured HUVECs were treated with 10 mg / L LPC for 24 hours The cell viability, the changes of MDA, NO and ROS were detected. Results: The model group with 10mg / L LPC compared with the control group showed that the cell culture supernatant MDA content was significantly increased, while the cell culture supernatant NO content was significantly reduced the level of reactive oxygen species Increased cell viability decreases. The experimental group and the model group found that 0.1μmol / L as the starting dose, in the range of 0.1 ~ 10.0μmol / L concentration range, and has a certain concentration-dependent relationship. With the increase of the effective concentration of the drug, the content of MDA in cell culture supernatant decreased significantly, the content of NO increased significantly, the level of reactive oxygen species decreased and the cell survival rate increased significantly. CONCLUSIONS: Stilbene glycoside can protect LEC-injured vascular endothelial cells by inhibiting the level of reactive oxygen species, increasing the production of NO and increasing the cell survival.