Recently, the function of blood cells in remote ischemic conditioning (RIC) mediated neuroprotection was undoubtedly confirmed. In the present paper, we have focused on the role of blood elements in glutamate homeostasis. The blood of remote conditioned (tolerant) animals was incubated ex vivo with 100 μM glutamate, and the quantitative and qualitative changes of excitatory amino acid transporters (EAAT 1, 2, and 3) were determined. We confirmed RIC mediated accelerated sequestration of extracellular glutamate via EAATs and altered distribution of that amino acid between plasma and cell elements compared to non-tolerant counterparts. The activity of EAATs was elevated in erythrocytes and monocytes, while the density of transporters was not affected. Quantitative changes of EAAT1 density were detected solely in platelets where the forced scavenging was independent of EAATs inhibition. Surprisingly, the trafficking of immunovisualised EAAT2 and 3 raised at tolerant erythrocytes and monocytes. We have found that protein synthesis underlined this process. On the other hand, depletion of protein synthesis did not significantly affect the scavenging capacity of those cell populations. Our work has demonstrated that the elevated blood scavenging of glutamate overdose could be one of the potential mechanisms underlying RIC mediated tissue protection.

最近，血细胞在远程缺血调节 (RIC) 介导的神经保护中的功能无疑得到了证实。在本文中，我们专注于血液元素在谷氨酸稳态中的作用。远程条件下（耐受）动物的血液在体外孵育用 100 μM 谷氨酸，测定兴奋性氨基酸转运蛋白（EAAT 1、2 和 3）的数量和质量变化。我们证实了 RIC 介导的细胞外谷氨酸通过 EAAT 加速螯合，并且与非耐受对应物相比，该氨基酸在血浆和细胞元件之间的分布发生了改变。EAATs 在红细胞和单核细胞中的活性升高，而转运蛋白的密度不受影响。EAAT1 密度的定量变化仅在血小板中检测到，其中强制清除与 EAAT 抑制无关。令人惊讶的是，免疫可视化 EAAT2 和 3 的贩运在耐受红细胞和单核细胞中升高。我们发现蛋白质合成强调了这个过程。另一方面，蛋白质合成的消耗并没有显着影响这些细胞群的清除能力。我们的工作表明，谷氨酸过量引起的血液清除率升高可能是 RIC 介导的组织保护的潜在机制之一。