Effect of Lianhuaqingwen capsules on inflammatory cytokines and junction protein expression in mice with acute lung injury induced by lipopolysaccharides / 中国药理学与毒理学杂志

ABSTRACT

OBJECTIVE To explore the effect of Lianhuaqingwen capsules ( LHQW ) on junction protein expression in mouse lung tissue of lipopolysaccharide (LPS)-induced acute lung injury ( ALl). METHODS 120 male mice were randomly divided into six groups normal control, model, model+dexa-methasone 5 mg.kg-1 , model +LHQW 2, 4 and 8 g.kg-1 groups. Dexamethasone and LHQW were administered orally, once daily, for 7 d. 24 h after the last administration, LPS solution was instilled into the tracheas of mice except the normal control group to prepare the mouse model of ALl. 24 h after the establishment of the ALl model, the mice were sacrificed and the pathological changes in the mouse lung tissue were observed by optical microscopy and ultrastructure of alveolar epithelium was observed by transmission electron microscopy. The cell percentage of positive expression of tumor necrosis factor-α(TNF-α) in the peripheral blood T lymphocytes was detected by flow cytometry. The expressions of con-nexin 43 ( Cx43), occludin and zonula occludens protein-1 ( ZO-1) in lung tissues were detected by immunohistochemistry. RESULTS Under the light microscope, the mouse lung of model group showed a large amount of inflammatory cell infiltration and alveolar wall thickening. Compared with model group, inflammatory cell infiltration was reduced in model+dexamethasone, model+LHQW 2,4 and 8 mg.kg-1 groups. Under the electron microscope, the mouse alveolar epithelial cells of model group showed injury. Compared with model group, the damage was reduced in model+dexamethasone, and model+LHQW 2, 4 and 8 mg.kg-1 groups. The cell percentage of TNF-α positive expression in peripheral blood T lympho-cytes in normal control, model, model+dexamethasone, model+LHQW 2,4 and 8 mg.kg-1 groups was (3.6±0.9)%, (6.4±0.8)%, (2.8±0.7)%, (4.7±1.6)%, (4.0±1.5)% and (3.6±1.2)%, respectively. The percentage in model group was obviously higher than that in normal control group( P<0.01), but was lower in the four drug treatment groups than in model group(P<0.05, P<0.01). The expression of Cx43, occludin and ZO-1 in lung tissue of model group was lower than that of normal control group(P<0.01), but higher in model+dexamethasone, model + LHQW 4 and 8 mg.kg-1 groups than in model group(P<0.05). CONCLUSION LHQW may alleviate ALl induced by LPS and play a protective role by inhibiting inflammatory cell infiltration and improving protein connection expression in alveolar epithelial cells and pulmonary vascular endothelial cells.