Xie Keliang, Wang Weina, Chen Hongguang, Han Huanzhi, Liu Daquan, Wang Guolin, Yu Yonghao
*Department of Anesthesiology, Tianjin Institute of Anesthesiology, General Hospital of Tianjin Medical University, Tianjin, China; †Department of Anesthesiology, Tianjin Hospital, Tianjin, China; and ‡Institute of Acute Abdominal Disease, Tianjin Nan Kai Hospital, Tianjin, China.
Shock. 2015 Jul;44(1):58-64. doi: 10.1097/SHK.0000000000000365.
Sepsis is the leading cause of death in critically ill patients. In recent years, molecular hydrogen, as an effective free radical scavenger, has been shown a selective antioxidant and anti-inflammatory effect, and it is beneficial in the treatment of sepsis. Rho-associated coiled-coil protein kinase (ROCK) participates in junction between normal cells, and regulates vascular endothelial permeability. In this study, we used lipopolysaccharide to stimulate vascular endothelial cells and explored the effects of hydrogen-rich medium on the regulation of adhesion of monocytes to endothelial cells and vascular endothelial permeability. We found that hydrogen-rich medium could inhibit adhesion of monocytes to endothelial cells and decrease levels of adhesion molecules, whereas the levels of transepithelial/endothelial electrical resistance values and the expression of vascular endothelial cadherin were increased after hydrogen-rich medium treatment. Moreover, hydrogen-rich medium could lessen the expression of ROCK, as a similar effect of its inhibitor Y-27632. In addition, hydrogen-rich medium could also inhibit adhesion of polymorphonuclear neutrophils to endothelial cells. In conclusion, hydrogen-rich medium could regulate adhesion of monocytes/polymorphonuclear neutrophils to endothelial cells and vascular endothelial permeability, and this effect might be related to the decreased expression of ROCK protein.
脓毒症是危重症患者死亡的主要原因。近年来，分子氢作为一种有效的自由基清除剂，已显示出选择性抗氧化和抗炎作用，对脓毒症治疗有益。Rho相关卷曲螺旋蛋白激酶（ROCK）参与正常细胞间连接，并调节血管内皮通透性。在本研究中，我们用脂多糖刺激血管内皮细胞，探讨富氢培养基对单核细胞与内皮细胞黏附及血管内皮通透性调节的影响。我们发现，富氢培养基可抑制单核细胞与内皮细胞的黏附并降低黏附分子水平，而富氢培养基处理后跨上皮/内皮电阻值水平及血管内皮钙黏蛋白表达增加。此外，富氢培养基可降低ROCK的表达，其效果与ROCK抑制剂Y-27632类似。另外，富氢培养基还可抑制多形核中性粒细胞与内皮细胞的黏附。总之，富氢培养基可调节单核细胞/多形核中性粒细胞与内皮细胞的黏附及血管内皮通透性，且这种作用可能与ROCK蛋白表达降低有关。
