• Xiaohua Guo, Zhenglian Wang, Yanan Liu, Qiulin Xu, Lei Su, and Fan Wu.
• Department of Pathophysiology of Southern Medical University, Key Laboratory of Shock and Microcirculation of Guangdong Province,Guangzhou 510515, China. E-mail: lanblue@smu.edu.cn.
• Nan Fang Yi Ke Da Xue Xue Bao. 2015 Aug 1; 35 (8): 1189-92, 1196.

ObjectiveTo investigate the molecular mechanisms of continuous venovenous hemofiltration (CVVH) combined with ulinastatin (ULI) (CVVH-ULI) for the treatment of septic shock.MethodsHuman umbilical endothelial cells (HUVECs) were incubated with serums isolated from normal healthy people (control), septic shock patients treated with conventional therapy (CT) or treated with CVVH combined with ULI (CVVH-ULI). Endothelial permeability was evaluated by the leakage of FITC-labeled albumin. The morphological changes of F-actin was evaluated by Rhodamine-phalloidin. The phosphorylated levels of p38 were determined by Western blot. Cells were then treated with p38inhibitor (SB203580), or DMSO, followed by incubation with serum from septic shock patients treated with conventional therapy. Endothelial permeability and F-actin rearrangements were also evaluated as noted above.ResultsSerum from CT group increased endothelial permeability, F-actin rearrangements, and phosphorylated levels of p38, which were inhibited by CVVH-ULI treatment. Moreover, in CT group, the serum-induced endothelial hyperpermeability and F-actin rearrangements were inhibited by SB203580, the inhibitor of p38.ConclusionCVVH combined with ulinastatin decreases endothelial hyperpermeability induced by septic shock through inhibiting p38 MAPK pathways.

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