Hiebert L M, Liu J M
Department of Physiology, University of Saskatchewan, Saskatoon, Canada.
Atherosclerosis. 1990 Jul;83(1):47-51. doi: 10.1016/0021-9150(90)90129-7.
Toxic oxygen metabolites can damage endothelial cells and may play an important role in the initiation and progression of atherosclerotic lesions. Since the antithrombotic drug heparin, interacts with endothelium, we wished to determine if heparin would protect endothelial cells from free radical injury. Endothelial cell injury was produced by the addition of xanthine and xanthine oxidase to cultured cells and assessed by changes in cell viability and release of lactate dehydrogenase (LDH) to the media. Pretreatment with heparin 24 h prior to addition of xanthine and xanthine oxidase significantly decreased cell damage. We suggest that heparin (and related compounds) can protect endothelium from free radical damage, and is therefore prophylactic for ischemic and inflammatory injury, and the development and progression of atheroma.
毒性氧代谢产物可损伤内皮细胞,并可能在动脉粥样硬化病变的发生和发展中起重要作用。由于抗血栓药物肝素可与内皮相互作用,我们希望确定肝素是否能保护内皮细胞免受自由基损伤。通过向培养细胞中添加黄嘌呤和黄嘌呤氧化酶来产生内皮细胞损伤,并通过细胞活力的变化和乳酸脱氢酶(LDH)释放到培养基中的情况进行评估。在添加黄嘌呤和黄嘌呤氧化酶前24小时用肝素预处理可显著减少细胞损伤。我们认为肝素(及相关化合物)可保护内皮免受自由基损伤,因此对缺血性和炎性损伤以及动脉粥样硬化的发生和发展具有预防作用。