Résumé
Objective To study the inflammation and expression of myosin light chain kinase(MLCK) through establishing acute lung injury animal model of mice induced by lipopolysacchride(LPS), and approach the role of MLCK in the mechanism of acute lung injury.Methods Twenty female BALB/c mice were randomly divided into LPS group(n=10) and control group(n=10).The BALB/c mice of LPS and control groups were induced by 30 ?L 0.9% NaCl via intranasal instillation,while only LPS group was treated with LPS(20 ?g/each mice).The pathology,wet/dry lung weight ratio and the total cell quantitation in bronchoalveolar lavage fluid(BALF)were compared between these two groups.Furthermore,immunohistochemistry assays were used to determine the status of MLCK expression in the lung.And RT-PCR was adopted to determine the status of MLCKmRNA in the lung. Results Compared with the control group,the LPS group showed more serious pulmonary hemorrhage,edema and infiltration of neutrophils, significantly increased water content in the lungs and total cell quantitation in BALF(P
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Objective To study the effect of montelukast(MK)and dexamethasone(Dex)on inflammation of asthma.Methods Asthma model was established and treated with MK or Dex.Bronchoalveolar lavage fluid(BALF) and histopathologic change were observed,IL-5mRNA of lung and bone marrow cells were detected by in situ hybridization,IL-5 immunoreactive cells by immunohistochemistry,and CD34+ and CD3+ of bone marrow cells by flow cytometry. ResultsCompared with asthma group,the number of total cells and eosinophils in BALF of MK group and Dex group were significantly decreased(P0.05). Conclusion MK and Dex can well inhibit airway inflammation and expression of IL-5mRNA in lung and bone marrow cells,though MK may be inferior to Dex in some aspects.The combined treatment of leukotriene receptor antagonist and glucocorticosteroid may be a new direction for asthma.
Résumé
Objective To study the expression of phosphorylated myosin light chain kinase(P-MLCK) in human pulmonary arterial endothelial cell(HPAEC) induced by lipopolysaccharide(LPS). Methods HPAECs were cultured in vitro and treated with LPS(2 ?g/mL) and normal saline for 1 h,respectively.Immunofluorescence method and western blotting were used to detect P-MLCK. Results Compared with normal saline group,the number of HPAECs decreased,but the morphology of cells did not change.After treatment of LPS for 30 and 60 min,the expression of P-MLCK in HPAEC increased from 0.41?0.05 to 0.82?0.43 and 1.56?0.07,respectively(P