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Chinese Journal of Digestion ; (12): 757-760, 2011.
Article in Chinese | WPRIM | ID: wpr-428191

ABSTRACT

Objective To establish Helicobacter pylori (Hp) infection induced chronic obstructive pulmonary disease (COPD) rat model,and to explore the role of Hp in the pathogenesis of COPD.Methods40 Wistar rats were randomly divided into double modeling group (Hp infection,smoked and intratracheal instillation of lipopolysaccharide),COPD group (smoked and intratracheal instillation of lipopolysaccharide),Hp infected group and control group.The lung function,cytokines level in serum and bronchial alveolar lavage fluid (BALF),Hp related genes expression in bronchial and lung tissue were detected.And Hp in bronchial and lung tissue was isolated and cultured.Results The lung tissue of both COPD group and double modeling group accorded with COPD pathological characteristics,and the latter was more apparent.The lung function of COPD group and double modeling group decreased more significantly than that of control group and Hp infected group (all P<0.05),and which was more obvious in double modeling group than that of COPD group (P<0.05).Along with the Hp colonization density increased,Ri and Re value of double modeling group increased (r=0.785 and 0.905),the value of Gdyn,PEF and FEV0.3/FVC decreased (r=-0.975,-0.959and -0.976).Compared with control group,IL-6,IL-8 and TNF-a cytokines levels in serum and bronchoalveolar lavage fluid of other groups increased significantly (all P<0.05),and within the groups,double modeling group increased most significantly (all P<0.05).Hp UreC gene was only amplified in part of bronchi and lung tissue of double modeling group,no Hp and suspicious bacteria colonies were isolated and cultured.ConclusionsHp not directly colonized in bronchi and lung tissue,which aggravated inflammation through increasing the serum and bronchoalveolar cytokines level of COPD rat model.Which caused the deterioration in lung function of COPD group.

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