Toborek M, Hennig B
Department of Nutrition and Food Science, University of Kentucky, Lexington 40506-0054.
Clin Chim Acta. 1993 Jun 16;215(2):201-11. doi: 10.1016/0009-8981(93)90126-o.
Disturbances in arterial wall elastin metabolism appear to be important factors in atherosclerosis development. To evaluate this hypothesis, elastase-like activity was determined in cultured endothelial cells and their surrounding media after exposure to tumor necrosis factor-alpha (TNF), cholestan-3 beta,5 alpha,6 beta-triol (Triol) and linoleic acid (18:2). Significant increases in elastase-like activity both in the cells and in the media were observed when subconfluent endothelial cells were treated with 12 microM Triol, 500 U TNF/ml, or 90 microM 18:2, for 72 h in the presence of 5% calf serum. Even higher activities were measured when endothelial cells were seeded directly into media enriched with 18:2, TNF or Triol and treated for 72 h. Vitamin E supplementation (25 microM) attenuated elastase-like activity in cells and media, independent of treatment. These results suggest that elastase-like enzyme induction in endothelial cells may be involved in cellular perturbations induced by certain lipids and cytokines. Vitamin E may provide a protective function by preventing the induction of elastolytic enzymes. This may have implications in elastin metabolism and atherosclerosis.
动脉壁弹性蛋白代谢紊乱似乎是动脉粥样硬化发展的重要因素。为了评估这一假设，在培养的内皮细胞及其周围培养基中，于暴露于肿瘤坏死因子-α（TNF）、胆甾烷-3β,5α,6β-三醇（三醇）和亚油酸（18:2）后测定类弹性蛋白酶活性。当在5%小牛血清存在的情况下，用12微摩尔三醇、500单位TNF/毫升或90微摩尔18:2处理亚汇合内皮细胞72小时时，观察到细胞和培养基中的类弹性蛋白酶活性均显著增加。当将内皮细胞直接接种到富含18:2、TNF或三醇的培养基中并处理72小时时，测得的活性更高。补充维生素E（25微摩尔）可减弱细胞和培养基中的类弹性蛋白酶活性，与处理方式无关。这些结果表明，内皮细胞中类弹性蛋白酶的诱导可能与某些脂质和细胞因子诱导的细胞扰动有关。维生素E可能通过防止弹性溶解酶的诱导发挥保护作用。这可能对弹性蛋白代谢和动脉粥样硬化有影响。
