Boissonneault G A, Hennig B, Wang Y, Wood C L
Department of Clinical Sciences, University of Kentucky, Lexington 40536.
Mech Ageing Dev. 1990 Oct;56(1):1-9. doi: 10.1016/0047-6374(90)90110-2.
As the endothelium ages it may become more susceptible to damage by atherogenic plasma components such as toxic lipid oxidation products. Vitamin E (vit E) might prove to be anti-atherogenic by reducing oxidative injury. This study investigated the effects of age and chronic exposure to fatty acid hydroperoxides (OFA) and/or vit E on endothelial barrier function (EBF) and cell growth characteristics. Chronic exposure to 5 microM OFA for 40 passages resulted in an age-related decrease in EBF, while supplementation of OFA-treated cultures with 25 microM vit E protected against the OFA-mediated decrease in EBF, independent of cell age. Vit E treatment alone had no significant effect on EBF relative to control cultures. No changes in growth characteristics, i.e., total DNA or protein per culture, were noted, regardless of treatment, although total DNA per culture decreased with increasing culture passage. These results suggest that chronic oxidative stress decreases EBF, predisposing the artery to infiltration by blood components and subsequent atherogenesis and that vit E delays cumulative changes in EBF related to chronic OFA exposure.
随着内皮细胞老化，它可能更容易受到动脉粥样硬化性血浆成分（如有毒脂质氧化产物）的损伤。维生素E（vit E）可能通过减少氧化损伤而具有抗动脉粥样硬化作用。本研究调查了年龄以及长期暴露于脂肪酸氢过氧化物（OFA）和/或vit E对内皮屏障功能（EBF）和细胞生长特性的影响。长期暴露于5 microM的OFA 40代导致EBF出现与年龄相关的下降，而在OFA处理的培养物中补充25 microM的vit E可防止OFA介导的EBF下降，且与细胞年龄无关。单独使用vit E处理相对于对照培养物对EBF没有显著影响。无论处理如何，均未观察到生长特性的变化，即每个培养物中的总DNA或蛋白质，尽管每个培养物中的总DNA随着传代次数的增加而减少。这些结果表明，慢性氧化应激会降低EBF，使动脉易受血液成分浸润及随后的动脉粥样硬化形成，并且vit E可延缓与长期OFA暴露相关的EBF累积变化。
