随着衰老,血管实际上会变得越来越好

  尽管许多年龄相关疾病的发病原因至今尚不清楚，但氧化性应激被认为是主要的罪魁祸首，氧化性应激被认为和心血管疾病和神经变性疾病，包括糖尿病、高血压及年龄相关的癌症直接相关；然而近日刊登在国际杂志The Journal of Physiology上的一篇研究论文中，来自密苏里的研究者发现，机体老化实际上可以提供明显的保护作用来抵御氧化性应激，相关研究发现表明，老化或许会诱发一种适应性反应来中和血管中氧化性应激的效应。
  研究者Steven Segal教授说道，名为活性氧自由基(ROS)的分子在调节细胞功能上扮演着重要作用，而ROS的过度产生则会产生一种被认为是氧化性应激的状况，氧化性应激会改变细胞的功能，并且干扰细胞的生长和繁殖。为了理解机体血管暴露于氧化性应激下老化对血管的功能的影响，研究者对小阻力动脉内皮进行了相关研究，阻力动脉对于心血管功能非常重要，因为其会调节血液流入组织的量以及全身性的血压。
  文章中研究者对4个月及24个月大的雄性小鼠的阻力动脉的内皮进行研究，小鼠两个年龄段相当于人类20岁出头及60开外；研究者首次在静息状态及氧化性应激不存在的情况下对阻力动脉内皮进行研究，随后通过加入过氧化氢来刺激产生氧化性应激，当氧化性应激被诱导20分钟后，相对于老年小鼠内皮细胞中的钙水平而言，年龄小鼠内皮细胞中的钙水平会发生异常性地增加，该研究非常重要，因为当钙质水平过高，细胞就会被严重损伤。
  当氧化性应激延长至60分钟，研究者发现，相比老年小鼠而言，年轻小鼠机体内皮细胞死亡的数量是前者的7倍，这就表明，随着年龄增加，当面临氧化性应激时内皮细胞就会不断适应去保护细胞的完整性；让研究者惊奇的是，相比于年龄小鼠，老年小鼠在氧化性应激条件下，其阻力动脉的内皮并不容易被干扰，本文研究发现，当机体不断衰老面临氧化性应激增加的情况下，机体血管就会产生适应性机制来调节ROS的水平，并且尽可能降低细胞的死亡，而这种适应性机制或可帮助解释为何老年个体的动脉仍然可以持续工作。
  尽管后期仍需要更多研究来鉴定内皮细胞随着机体老化不断适应的机制，然而本文研究就已经表明，当个体衰老时，其机体的自然趋势是选择更易于去适应氧化性应激的方式。（转化医学网360zhyx.com）
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转化医学网推荐的原文摘要：

Advanced age protects microvascular endothelium from aberrant Ca2+ influx and cell death induced by hydrogen peroxide
The Journal of Physiology    DOI: 10.1113/JP270169
Matthew J. Socha1, Erika M. Boerman1, Erik J. Behringer1, Rebecca L. Shaw1, Timothy L. Domeier1 andSteven S. Segal1,2,*
Endothelial cell Ca2+ signalling is integral to blood flow control in the resistance vasculature yet little is known of how its regulation may be affected by advancing age. We tested the hypothesis that advanced age protects microvascular endothelium by attenuating aberrant Ca2+ signalling during oxidative stress. Intact endothelial tubes (width, ∼60 μm; length, ∼1000 μm) were isolated from superior epigastric arteries of Young (3–4 months) and Old (24–26 months) male C57BL/6 mice and loaded with Fura-2 dye to monitor [Ca2+]i. At rest there was no difference in [Ca2+]i between age groups. Compared to Young, the [Ca2+]i response to maximal stimulation with acetylcholine (3 μm, 2 min) was ∼25% greater in Old, confirming signalling integrity with advanced age. Basal H2O2 availability was ∼33% greater in Old while vascular catalase activity was reduced by half. Transient exposure to elevated H2O2 (200 μm, 20 min) progressively increased [Ca2+]i to ∼4-fold greater levels in endothelium of Young versus Old. With no difference between age groups at rest, Mn2+ quench of Fura-2 fluorescence revealed 2-fold greater Ca2+ influx in Young during elevated H2O2; this effect was attenuated by ∼75% using ruthenium red (5 μm) as a broad-spectrum inhibitor of transient receptor potential channels. Prolonged exposure to H2O2 (200 μm, 60 min) induced ∼7-fold greater cell death in endothelium of Young versus Old. Thus, microvascular endothelium can adapt to advanced age by reducing Ca2+ influx during elevated oxidative stress. Protection from cell death during oxidative stress will sustain endothelial integrity during ageing.