Effect of 15d-PGJ2 on endotoxin-induced acute lung injury in rats / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effect of 15-deoxy-△12,14-prostaglandin J2 (15d-PGJ2) on endotoxin-induced acute lung injury (ALI) in rats.Methods Forty healthy male Sprague-Dawley rats, aged 3-5 months, weighing 220-250 g, were randomly divided into 4 groups (n =10 each) using a random number table control group (group C), 15d-PGJ2 group, lipopolysaccharide (LPS) group, and LPS +15d-PGJ2 group.In group 15d-PGJ2, 15d-PGJ20.3 mg/kg was injected via the tail vein, while the equal volume of normal saline was given in group C.In LPS and LPS+15d-PGJ2 groups, ALI was produced with LPS 6 mg/kg injected through the tail vein, and then the equal volume of normal saline and 15d-PGJ2 0.3 mg/kg were injected, respectively.At 4 h after LPS injection, blood samples were drawn from the abdominal aorta for blood gas analysis, and arterial oxygen partial pressure (PaO2) was recorded.The rats were then sacrificed, lungs were removed for microscopic examination, and for determination of wet/dry lung weight ratio (W/D ratio), TNF-α, IL-8 and cytokine-induced neutrophil chemoattractant-1 (CINC-1) contents (by enzyme-linked immunosorbent assay) , and nuclear factor kappa B (NF-κB) p65 and IκB-α expression (by Western blot).Results Compared with group C, no significant change was found in PaO2, W/D ratio, contents of TNF-α, IL-8 and CINC-1, and expression of NF-κB p65 and IκB-α in group 15d-PGJ2 (P＞0.05), and PaO2 was significantly decreased, W/D ratio and contents of TNF-α,IL-8 and CINC-1 were increased, the expression of NF-κB p65 was up-regulated, and the expression of IκB-α was down-regulated in LPS and LPS+ 15d-PGJ2 groups (P＜0.05).Compared with group LPS,PaO2 was significantly increased, W/D ratio and contents of TNF-α, IL-8 and CINC-1 were decreased, the expression of NF-κB p65 was down-regulated, and the expression of IκB-α was up-regulated (P＜0.05),and the pathological changes were attenuated in group LPS+ 15d-PGJ2.Conclusion 15d-PGJ2 can mitigate endotoxin-induced ALI in rats.