目的研究油茶皂苷(SQS)对缺氧-复氧诱导的内皮细胞损伤及中性粒细胞黏附的作用及可能的机制。方法建立人脐静脉内皮细胞(HUVEC)缺氧-复氧损伤模型,取培养细胞上清液测定LDH活性,分别测定HU-VEC存活率,中性粒细胞黏附率、线粒体丙二醛(MDA)水平及超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性。同法检测中性粒细胞黏附。结果缺氧-复氧可导致HUVEC损伤及中性粒细胞黏附的增加,表现为LDH活性、MDA水平及中性粒细胞黏附率显著升高,而SOD和GSH-Px活性显著下降;SQS呈浓度依赖性地对抗上述改变。结论SQS对缺氧-复氧诱导的HUVEC损伤有保护作用,其机制可能与其抗脂质过氧化和抑制白细胞黏附有关。

Objective To investigate the effect of sasanquasaponin (SQS) on injury of endothelial cells induced by hypoxia-reoxygenation and neutrophil adhesion, and its possible mechanisms. Methods Human umbilical vein endothelial cells (HUVEC) were exposed to normoxia or hypoxia-reoxygenation in the absence or presence of SQS (10.0, 1.0, and 0.1 μmol/L). Lactate dehydrogenase (LDH) activity was determined in cultured HUVEC supernatants. HUVEC survival rate, neutrophil adhesion rate, malondialdehyde (MDA) level superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were measured. Neutrophil adhesion was assayed in additional HUVEC treated as above. Results The results showed that hypoxia-reoxygenation resulted in HUVEC injury and enhancement of neutrophil adhesion, with the increase in LDH activity, MDA level, and adhesion rate as well, conversely, with the decrease in activity of SOD and GSH-Px; SQS antagonized these changes in a concentration-dependent manner. Conclusion SQS may protect HUVEC against hypoxia-reoxygenation injury and its mechanism appeares to be related to anti-lipoperoxidization and anti-adhesion of white blood cell.

江西省自然科学基金资助项目(0140030)