Tao Bingdong, Liu Lidan, Wang Ni, Wang Wei, Jiang Jingjing, Zhang Jin
Department of Anesthesiology, Shengjing Hospital, China Medical University, Shenyang, People's Republic of China.
Department of Anesthesiology, Shengjing Hospital, China Medical University, Shenyang, People's Republic of China.
J Surg Res. 2016 May 15;202(2):291-8. doi: 10.1016/j.jss.2016.01.009. Epub 2016 Jan 14.
Aquaporin 1(AQP1) and AQP5 have an important role in eliminating extravascular lung water, an increase of which contributes to lung injury in patients with sepsis and its consequent mortality. It has been reported that hydrogen-rich saline (HRS) has protective effects against sepsis-related lung injury. In this study, we hypothesized that the protective effect occurred by preserving the expression of AQP1 and AQP5. To test this hypothesis, male Sprague-Dawley rats received intratracheal administration of lipopolysaccharide (LPS) followed by intraperitoneal injection of HRS. Lung function, wet-to-dry weight ratio, and histopathology scores were determined. The expression of AQP1 and AQP5 at the messenger RNA and protein levels, as well as the involved pathways, was explored by quantitative polymerase chain reaction and Western blot. LPS significantly impaired lung function and downregulated the expression of AQP1 and AQP5 in the rat lung, all of which were attenuated by HRS treatment. Moreover, HRS treatment inhibited LPS-induced activation of p38 mitogen-activated protein kinase and jun N-terminal kinase, which is associated with LPS-induced downregulation of AQP1 and AQP5.
水通道蛋白1（AQP1）和水通道蛋白5在清除血管外肺水方面发挥着重要作用，血管外肺水增加会导致脓毒症患者发生肺损伤及其随后的死亡。据报道，富氢盐水（HRS）对脓毒症相关肺损伤具有保护作用。在本研究中，我们假设这种保护作用是通过维持AQP1和AQP5的表达而产生的。为验证这一假设，对雄性Sprague-Dawley大鼠进行气管内注射脂多糖（LPS），随后腹腔注射HRS。测定肺功能、湿重与干重比以及组织病理学评分。通过定量聚合酶链反应和蛋白质印迹法探究AQP1和AQP5在信使核糖核酸和蛋白质水平的表达以及相关途径。LPS显著损害大鼠肺功能并下调大鼠肺中AQP1和AQP5的表达，而所有这些均因HRS治疗而减轻。此外，HRS治疗抑制了LPS诱导的p38丝裂原活化蛋白激酶和Jun氨基末端激酶的激活，这与LPS诱导的AQP1和AQP5下调有关。
