RÉSUMÉ
Objective To investigate of effect and mechanism of honokiol against acute lung injury (ALI) induced by lipopolysaccharide (LPS).Methods Forty SPF BALB/c mice were randomly divided into 5 groups (N =8),normal control group,LPS group,low-and high-dose magnolol groups,and dexamethasone group.The mouse model of ALI was induced by LPS.After intraperitoneal injection of honokiol,we detected neutrophil count,concentration of albumin,and pulmonary myeloperoxidase (MPO) activity in bronchoalveolar lavage fluid (BALF)as well as alveolar permeability.We also detected the levels of malondialdehyde (MDA),protein carbonyl content(PCC),reactive oxygen species (ROS) and glutathione(CAT),and the activities of superoxide dismutase (SOD),catalase,glutathione peroxidase (GPx),and glutathione-S-transferase(GST) in lung tissue of mice.Results In the LPS group,the neutrophil count,albumin concentration,MPO activity and Evans blue (EB)content were increased (P ＜ 0.05),and anti-oxidase activity was decreased significantly (P ＜ 0.05).After treatment with honokiol,the neutrophil count,albumin concentration,MPO activity,EB content,and lipid peroxidation level were decreased significantly,and the activities of antioxidant enzymes were increased significantly (P ＜ 0.05).Conclusion Honokiol has protective effects against LPS-induced acute lung injury through inhibiting oxidative stress.
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Objective To explore the regulatory effect of Nervilia fordii Injection ( NFI ) on inflammatory cytokines in rats with lipopolysaccharide ( LPS) -induced acute lung injury ( ALI) , and to explore its possible interfering mechanism . Methods The rats were randomly divided into normal group , model group , Shenmai Injection group, and NFI group. J774 macrophages were stimulated by LPS to establish the cell model in vitro, and in vivo ALI rat model was established by injection of LPS through the sublingual veins. Electronic microscope and enzyme-linked immunosorbent assay (ELISA) were used for observing the proliferation of J774 macrophages, the levels of supernatant inflammatory cytokines secreted by J774 cells, and the levels of serum inflammatory cytokines . Results The proliferation of LPS-induced J774 macrophages was increased , and the secretion of inflammatory cytokines was disordered. Uncontrolled inflammatory reaction occurred in the lung after the rats were administrated with intravenous injection of LPS . Both NFI and Shenmai Injection could inhibit the proliferation of J774 macrophages. NFI could also significantly inhibit the levels of supernatant and serum tumor necrosis factor (TNF) -α and interleukin 6 (IL-6) expression (P0.05). Conclusion NFI has better preventive and therapeutic effect for ALI than Shenmai Injection, and its possible mechanism is related with the inflammatory regulation and lung injury relief through the suppression of excessive expression of TNF-α and IL-6 .
RÉSUMÉ
Objective To investigate the therapeutic mechanism of Shengjiang Powder(SP)on acute lung injury.Methods Forty healthy SD male rats were divided into 3 groups randomly: normal group,model group,and SP group.After administration for 6 days,acute lung injury rat models were established by injecting lipopolysaccharide(LPS)into sublingual vein.Lung histological sections were prepared for the detection of NF-?B expression by immmunohistochemistry.The images of the lung histological sections were captured and the average gray values of nucleus of endothelial cells in lung micrangium were measured.Results Compared with the model group,SP could depress the expression of NF-?B in the nucleus of lung microvascular endothelial cells,and statistical difference existed between the two groups(P