Department of Anesthesiology, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai 200032, China.
Cell Biochem Biophys. 2011 Sep;61(1):123-9. doi: 10.1007/s12013-011-9168-6.
Preconditioning with sevoflurane (SPC) diminishes effusion of rat alveolar membrane during inflammation. It is not clear whether this preconditioning directly inhibits permeability of pulmonary microvascular endothelial cell (PMVEC) monolayer. In this article, we evaluated effects of SPC on permeability of PMVEC monolayer and identified signaling pathways involved in these effects. PMVEC monolayer was exposed to different conditions (5-hydroxydecanoate (5-HD), TNF-α, SPC, SPC with subsequent exposure to TNF-α and 5-HD, and SPC with subsequent exposure to TNF-α alone), and the permeability of PMVEC monolayer was assessed using FITC-bovine serum albumin (ELISA). Expression of ICAM-1 (Western blot and RT-PCR) and activation of p38 MAPK (Western blot) were also assessed. Compared to the TNF-α group, permeability of PMVEC monolayer in the SPC + TNF-α group was significantly lower. Activation of p38 MAPK was also diminished in the TNF-α group. Pre-treatment with 5-HD reverted beneficial effects of SPC. Expression of ICAM-1 was not modulated by any of the tested experimental exposures. The results of this study demonstrate that SPC is capable of diminishing the TNF-α-induced increase of permeability of PMVEC monolayer, and that this beneficial effect is partly reversed by 5-HD. Further, SPC suppresses activation of p38 MAPK.
七氟醚预处理（SPC）可减轻炎症期间大鼠肺泡膜的渗出。目前尚不清楚这种预处理是否直接抑制肺微血管内皮细胞（PMVEC）单层的通透性。在本文中，我们评估了 SPC 对 PMVEC 单层通透性的影响，并确定了涉及这些作用的信号通路。将 PMVEC 单层暴露于不同条件下（5-羟基癸酸（5-HD）、TNF-α、SPC、随后暴露于 TNF-α和 5-HD 的 SPC 以及随后单独暴露于 TNF-α的 SPC），并使用 FITC-牛血清白蛋白（ELISA）评估 PMVEC 单层的通透性。还评估了 ICAM-1 的表达（Western blot 和 RT-PCR）和 p38 MAPK 的激活（Western blot）。与 TNF-α 组相比，SPC+TNF-α 组的 PMVEC 单层通透性明显降低。TNF-α 组中 p38 MAPK 的激活也减弱。5-HD 的预处理逆转了 SPC 的有益作用。ICAM-1 的表达不受任何测试实验暴露的调节。本研究结果表明，SPC 能够降低 TNF-α诱导的 PMVEC 单层通透性增加，而这种有益作用部分被 5-HD 逆转。此外，SPC 抑制了 p38 MAPK 的激活。
