Skip to main content
Fig. 3 | Respiratory Research

Fig. 3

From: The HDL from septic-ARDS patients with composition changes exacerbates pulmonary endothelial dysfunction and acute lung injury induced by cecal ligation and puncture (CLP) in mice

Fig. 3

The plasma HDL from ARDS patients promotes CLP-induced ALI in apoA-I KO mice with the deficiency of endogenous HDL. a A depleted level of plasma HDL is observed in apoA-I KO mice and the moderate CLP surgery caused a marked decrease in the level of plasma HDL in WT mice (n = 5–8 per group). b Representative hematoxylin and eosin–stained lung sections from apoA-I KO mice treated with PBS, N-HDL or A-HDL after light CLP. c The degree of lung injury (n = 7 per group). d The ratio of lung wet/dry weight (n = 5 per group). e The level of TNF-α in BALF after CLP (n = 5 per group). f The mRNA expressions of pro-inflammatory cytokines (TNF-a, IL-1 and MCP1) in lung tissues by qPCR analyses (n = 5 per group). g The level of plasma LPS after CLP surgery (n = 5–8 per group). **p < 0.01 versus sham group of WT mice and ####p < 0.0001 versus sham group in a. *p < 0.05 and **p < 0.01 versus sham group; #p < 0.05, ##p < 0.01 versus PBS treatment group; &p < 0.05 and &&p < 0.01 versus N-HDL treatment group in c to g. CLP: Cecal ligation and puncture, N-HDL: HDL from normal subjects, A-HDL: HDL from ARDS patients. Scale bar: 100 μm

Back to article page