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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Restoration of endothelin-1-induced impairment in endothelium-dependent relaxation by interleukin-10 in murine aortic rings.
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Restoration of endothelin-1-induced impairment in endothelium-dependent relaxation by interleukin-10 in murine aortic rings.

机译：白介素-10在鼠主动脉环中内皮素-1诱导的内皮依赖性舒张损伤的恢复。

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Endothelin-1 (ET-1) is implicated in the development of endothelial dysfunction through the generation of reactive oxygen species by NADPH oxidase activation. Interleukin-10 (IL-10) is an antiinflammatory cytokine that stimulates nitric oxide production, decreases superoxide production, and restores endothelial integrity after vascular injury. In this study, we tested whether IL-10 attenuates ET-1-induced endothelial dysfunction by improving acetylcholine (ACh)-induced relaxation of cultured murine aortic rings. Aortic rings (2 mm long) of C57BL/6 mice were incubated in 2 mL DMEM containing 120 U/mL penicillin and 120 microg/mL streptomycin in the presence of one of 4 treatments: vehicle (deionized water), ET-1 (100 nmol/L), recombinant mouse IL-10 (300 ng/mL), or a combination of both ET-1 and IL-10. After incubation at 37 degrees C for either 1 or 6 h (short-term exposure) or 22 h (overnight exposure), rings were mounted in a wire myograph and stretched to a passive force of 5 mN. Endothelium-dependent vasorelaxation was assessed by constructing cumulative concentration-response curves to ACh (0.001-10 micromol/L) during 10 mumol/L phenylephrine (PE)-induced contraction. Short-term exposure of ET-1 did not result in an impairment of ACh-induced relaxation. Overnight exposure of aortic rings to ET-1 resulted in a statistically significant endothelial dysfunction characterized by a reduced maximal relaxation response to ACh compared with that of untreated rings (Emax 57% +/- 3% versus 82% +/- 4%). IL-10 treatment restored ACh-induced relaxation (Emax 77% +/- 3%). Western blotting showed decreased eNOS expression in response to ET-1, whereas vessels treated with a combination of ET-1 and IL-10 showed increased expression of eNOS. Immunohistochemical analysis showed decreased eNOS expression in ET-1-treated vessels compared with those treated with both ET-1 and IL-10. We conclude that, in murine aorta, the antiinflammatory cytokine IL-10 prevents impairment in endothelium-dependent relaxation induced in response to long-term incubation with ET-1 via normalization of eNOS expression.
机译：内皮素-1（ET-1）通过NADPH氧化酶活化产生活性氧而参与内皮功能障碍的发展。白细胞介素10（IL-10）是一种抗炎细胞因子，可刺激一氧化氮的产生，减少超氧化物的产生并在血管损伤后恢复内皮的完整性。在这项研究中，我们测试了IL-10是否通过改善乙酰胆碱（ACh）诱导的培养的鼠主动脉环的松弛来减轻ET-1诱导的内皮功能障碍。将C57BL / 6小鼠的主动脉环（长2毫米）在2种含有120 U / mL青霉素和120 microg / mL链霉素的DMEM中进行以下4种处理之一进行孵育：溶媒（去离子水），ET-1（100） nmol / L），重组小鼠IL-10（300 ng / mL）或ET-1和IL-10的组合。在37摄氏度下孵育1或6小时（短期暴露）或22小时（过夜暴露）后，将环安装在钢丝肌动描记器中，并拉伸至5 mN的被动力。通过构建10μmol/ L苯肾上腺素（PE）诱导的收缩期间对ACh（0.001-10 micromol / L）的累积浓度-响应曲线，评估内皮依赖性血管舒张。短期暴露于ET-1不会导致ACh诱导的舒张功能受损。过夜暴露于ET-1的主动脉​​环导致统计学上显着的内皮功能障碍，其特征是与未处理的环相比，对ACh的最大舒张反应降低（Emax为57％+/- 3％对82％+/- 4％）。 IL-10治疗可恢复ACh诱导的舒张作用（Emax 77％+/- 3％）。 Western印迹显示响应ET-1的eNOS表达降低，而用ET-1和IL-10组合处理的血管显示eNOS表达增加。免疫组织化学分析显示，与经ET-1和IL-10处理的血管相比，经ET-1处理的血管中eNOS表达降低。我们得出的结论是，在鼠主动脉中，抗炎细胞因子IL-10可以通过eNOS表达的正常化来防止因与ET-1长期孵育而引起的内皮依赖性舒张损伤。

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