RESUMO
Objective:To investigate the effects of lipopolysaccharide (LPS)on the acute lung injury (ALI)and expressions of aquaporin 1 (AQP1)and aquaporin 5 (AQP5)in lung tissue of the rats. Methods:Forty-eight SPF grade male Wistar rats were randomly divided into control group and LPS group (n=24).The rats in LPS group were intravenously injected with LPS to induce ALI models,and the rats in control group were injected with saline. The rats were sacrificed at 2,6,12 and 24 h,and the samples were collected after the successful modeling.The pathological changes of lung tissue were observed with HE staining;the lung wet/dry weight (W/D)ratio and lung permeability index were detected;ELISA was used to detect the levels of TNF-αand MIP-1α.The expression levels of AQP1 and AQP5 protein and mRNA were measured by Western blotting,immunohistochemistry and Real-Time PCR methods. Results:Compared with control group, the TNF-α and MIP-1α levels in LPS group were significantly elevated at 2,6 and 12 h (P<0.05),and at 24 h they were gradually reduced to the normal level. The HE staining results showed the alveolar and interstitial edema at 2 h after LPS injection,obviously in 12 h. The lung W/D ratios and pulmonary permeability indexes at different time points in LPS group were significantly higher than those in control group (P<0.05),and they reached the peak at 12 h.The expression levels of AQP1 and AQP5 mRNA and protein in lung tissue of the rats at different time points in LPS group were significantly lower than those in control group (P<0.01 ). Conclusion:LPS can induce ALI in the rats and down-regulate the expressions of AQP1 and AQP5;LPS is involved in the formation of pulmonary edema.
RESUMO
Objective To investigate the protective role of losartan,an angiotensin Ⅱ receptor(AT1 type)blocker,in the mechanical ventilation-induced lung injury(VILI).Methods Forty Sprague-Dawley rats weighing 300-350 g were randomly divided into the following four experimental groups(10 rats in each group):control group(group A),normal tidal volume venti-lation group(group B),large tidal volume mechanical ventilation group(group C),large tidal volume mechanical ventilation plus Losartan pretreatment group(group D).The pulmonary tissues were removed for pathological examination and detection of NF-κB activity,and the lung lavage fluid was collected for analysis of white blood cell count,total protein concentration and the level of MIP-2,after the rats were sacrificed.Results The pathology of lung tissues was normal in groups A and B.There was obvi-ous inflammatory damage in lung tissues in group C.The pathological inj uries of lung tissue were significantly reduced in group D compared with group C.The NF-κB activity and the level of p65 were significantly higher in group C than in groups A and B (P<0.01);they were significantly reduced in group D compared with group C(P<0.05).Total protein concentration,the MIP-2 level and the white blood cell count were significantly higher in group C than in groups A and B(P<0.01).They were significantly reduced in group D compared with group C(P<0.05 or 0.01).Conclusion Losartan,a selective inhibitor of sub-type AT1 receptors for angiotensin Ⅱ,can relieve VILI by inhibiting the activity of NF-κB.
