Abstract:The protective effects of sasanquasaponin, an effective compound from Chinese traditional herbs, on ischaemia and reperfusion injury in mouse hearts have been suggested through modulation of intracellular Cl -homeostasis. The effects of sasanquasaponin on injury of endothelial cells, however, induced by anoxia and reoxygenation remain unknown. Therefore, the present study attempted to observe the effects of sasanquasaponin on anoxia and reoxygenation injury in endothelial cells and investigate its putative mechanisms. Human umbilical vein endothelial cells (HUVECs) were exposed to normoxia or anoxia and reoxygenation in the absence or presence of sasanquasaponin (10.0, 1.0 and 0.1 μ mol / l). Lactate dehydrogenase activity was determined in cultured HUVECs supernatant, and malondialdehyde content, superoxide dismutase and glutathione peroxidase activities were measured in HUVECs by a colorimetric method. Neutrophil adhesion to HUVECs was assayed colorimetrically. The levels of intercellular adhesion molecule-1 and tumour necrosis factor-α were detected. The activity of nuclear factor kappa B was determined by flow cytometry. The results show that sasanquasaponin decreased the lactate dehydrogenase activity and malondialdehyde contents, and inhibited the neutrophil adhesion to HUVECs; sasanquasaponin, moreover, inhibited nuclear factor kappa B transnuclear activity, lowered tumour necrosis factor-α and intercellular adhesion molecule-1 expression levels. On the other hand, sasanquasaponin increased the mitochondrial superoxide dismutase and glutathione peroxidase activities. It is suggested that sasanquasaponin could protect HUVECs against anoxia and reoxygenation injury, and the protective mechanisms appear to be related to anti-lipoperoxidation and anti-adhesion.Ischaemia and reperfusion are likely to play an important role in the pathogenesis of a wide variety of clinical conditions such as peripheral vascular disease, stroke and myocardial infarction [1,2]. Adhesion of leucocytes to endothelial cells is involved in the progression of these diseases. There is much evidence that neutrophil adhesion is a critical factor in ischaemia and reperfusion injury, and vascular endothelium is a crucial site of ischaemia and reperfusion injury [3,4]. Data have shown that endothelial cells, under ischaemic or hypoxic conditions, present dysfunction of energy metabolism, overload of intracellular Ca 2+ concentration ([Ca 2+

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