The protective effect of interleukin-10 on lipopolysaccharide-induced acute lung injury in rats by attenuating the release of extracellular high mobility group protein 1

Abstract

Objective This study aimed to investigate the effect of interleukin (IL)-10 on extracellular release of high mobility group protein 1 (HMGB1) in lipopolysaccharide (LPS)-induced acute lung injury in rats and its possible mechanism.Methods LPS (5 mg/kg,ip) induced acute lung injury model was used in our experiment,the healthy male Sprague-Dawley rats,weighed 180 g-220 g,were randomly divided into four groups:control group only used phosphate buffered solution (PBS) (group P,n=6),PBS+IL-10 group (group PI,n=6),acute lung injury group also LPS group (group L,n=30),LPS+interleukin-10 group(group LI,n=30).In the group L and LI,4,8,16,24 h and 48 h after the injection of LPS,the lung wet/dry weight ratio(W/D) and the concentration of the total protein in bronchoalveolar lavage fluid (BALF) were analyzed.The cytokines [tumor necrosis factor-α(TNF-α) and IL-6] in bronchoalveolar lavage fluid were detected by enzyme-linked immunosorbent assay.Hitophathological changes in lung tissue were observed by hematoxylin-eosin staining,and the expression of HMGB1 was analyzed by Western Blot.Results After using of LPS,the W/D and the concentration of the total protein in BALF in group L were (5.68±0.12) mg/L and (254± 105)mg/L,which were increased by 12％ and 297％(P＜0.05),compared with the group P,the concentration of TNF-α and IL-6 in BALF,HE staining of the lung tissue infiltration and the expression of HMGB1 in the lung tissue were all increased (P＜0.05).However after the intratracheal spray of IL-10,the W/D and the concentration of the total protein in BALF in group LI were (5.28±0.14) mg/L and (109±48) mg/L,which were decreased by 7％ and 57％(P＜0.05),compared with the group L,the level of inflammatory factors,lung tissue infiltration and the concentration of HMGB1 were all decreased (P<0.05).Conclusions IL-10 can attenuate the injury induced by LPS in acute lung injury.The mechanism may be due to the effect of decreasing the proinflammatory cytokines and down-regulating the expression of HMGB1. Key words: Interleukin-10; Lipopolysaccharide; Acute lung injury; High mobility group protein 1