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Mechanism of intestinal mucosal barrier dysfunction in a rat model of chronic obstructive pulmonary disease: An observational study

View Article: PubMed Central - PubMed

ABSTRACT

The aim of the present study was to investigate intestinal mucosal barrier dysfunction in a rat model of chronic obstructive pulmonary disease (COPD). Male Sprague Dawley rats (n=40) were evenly randomized into control and COPD groups and the COPD model was established by regulated exposure to cigarette smoke for 6 months. Histopathological changes of the lung and intestinal tissues were detected by hematoxylin and eosin staining. Expression of the tight junction proteins occludin and zona occludens-1 (ZO-1) in the intestinal tissues were analyzed by western blotting, serum diamine oxidase (DAO) activity was detected by spectrophotometry, the urinary lactulose to mannitol ratio (L/M) was evaluated by high performance liquid chromatography, and intestinal tissue secretion of tumor necrosis factor (TNF)-α, interferon (IFN)-γ and interleukin (IL)-8 were detected by ELISA. Lung histopathology revealed thinned alveolar walls, ruptured alveolar septa, enlarged and deformed alveoli, and the formation of bullae and emphysema due to alveolar fusion in the COPD group, while intestinal histopathology indicated clearly swollen intestines with darkened and gray mucosa, neutrophil infiltration of the intestinal mucosal and regional epithelial shedding. The occludin and ZO-1 expression levels were significantly lower in the COPD group compared with those in the corresponding control group (P<0.05), while the urinary L/M ratio was significantly higher (P<0.05). Furthermore, the serum DAO activity and secretion of TNF-α, IFN-γ and IL-8 in the intestinal tissues were significantly higher in the COPD group than in the control group (each P<0.05). Dysfunctional and structural changes were observed in the intestinal mucosal barrier in COPD model rats, which may be associated with the increased intestinal inflammatory responses.

No MeSH data available.


Related in: MedlinePlus

Lung tissue of a rat from the chronic obstructive pulmonary disease group, which exhibited lesions, characterized by a thinned alveolar wall, ruptured alveolar septa, enlarged and deformed alveoli, and formation of bullae due to alveolar fusion. Hematoxylin and eosin staining; moderate magnification (×100).
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f2-etm-0-0-3493: Lung tissue of a rat from the chronic obstructive pulmonary disease group, which exhibited lesions, characterized by a thinned alveolar wall, ruptured alveolar septa, enlarged and deformed alveoli, and formation of bullae due to alveolar fusion. Hematoxylin and eosin staining; moderate magnification (×100).

Mentions: The lung histopathology indicated normal pulmonary structures, an absence of inflammatory infiltration in the small airways and structural integrity of the alveolar wall (Fig. 1) in the control group. However, in the COPD group, a large amount of monocyte and lymphocyte infiltration at and around the small airway walls was observed, with thinning of the alveolar wall, ruptured alveolar septa, interstitial pulmonary congestion and edema, reduced blood vessel density, enlarged and deformed alveoli, and formation of bullae due to alveolar fusion (Fig. 2). These results indicated the presence of emphysema and other pathological changes in the rats from the COPD group and confirmed the successful establishment of the rat model of COPD.


Mechanism of intestinal mucosal barrier dysfunction in a rat model of chronic obstructive pulmonary disease: An observational study
Lung tissue of a rat from the chronic obstructive pulmonary disease group, which exhibited lesions, characterized by a thinned alveolar wall, ruptured alveolar septa, enlarged and deformed alveoli, and formation of bullae due to alveolar fusion. Hematoxylin and eosin staining; moderate magnification (×100).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4997986&req=5

f2-etm-0-0-3493: Lung tissue of a rat from the chronic obstructive pulmonary disease group, which exhibited lesions, characterized by a thinned alveolar wall, ruptured alveolar septa, enlarged and deformed alveoli, and formation of bullae due to alveolar fusion. Hematoxylin and eosin staining; moderate magnification (×100).
Mentions: The lung histopathology indicated normal pulmonary structures, an absence of inflammatory infiltration in the small airways and structural integrity of the alveolar wall (Fig. 1) in the control group. However, in the COPD group, a large amount of monocyte and lymphocyte infiltration at and around the small airway walls was observed, with thinning of the alveolar wall, ruptured alveolar septa, interstitial pulmonary congestion and edema, reduced blood vessel density, enlarged and deformed alveoli, and formation of bullae due to alveolar fusion (Fig. 2). These results indicated the presence of emphysema and other pathological changes in the rats from the COPD group and confirmed the successful establishment of the rat model of COPD.

View Article: PubMed Central - PubMed

ABSTRACT

The aim of the present study was to investigate intestinal mucosal barrier dysfunction in a rat model of chronic obstructive pulmonary disease (COPD). Male Sprague Dawley rats (n=40) were evenly randomized into control and COPD groups and the COPD model was established by regulated exposure to cigarette smoke for 6 months. Histopathological changes of the lung and intestinal tissues were detected by hematoxylin and eosin staining. Expression of the tight junction proteins occludin and zona occludens-1 (ZO-1) in the intestinal tissues were analyzed by western blotting, serum diamine oxidase (DAO) activity was detected by spectrophotometry, the urinary lactulose to mannitol ratio (L/M) was evaluated by high performance liquid chromatography, and intestinal tissue secretion of tumor necrosis factor (TNF)-α, interferon (IFN)-γ and interleukin (IL)-8 were detected by ELISA. Lung histopathology revealed thinned alveolar walls, ruptured alveolar septa, enlarged and deformed alveoli, and the formation of bullae and emphysema due to alveolar fusion in the COPD group, while intestinal histopathology indicated clearly swollen intestines with darkened and gray mucosa, neutrophil infiltration of the intestinal mucosal and regional epithelial shedding. The occludin and ZO-1 expression levels were significantly lower in the COPD group compared with those in the corresponding control group (P<0.05), while the urinary L/M ratio was significantly higher (P<0.05). Furthermore, the serum DAO activity and secretion of TNF-α, IFN-γ and IL-8 in the intestinal tissues were significantly higher in the COPD group than in the control group (each P<0.05). Dysfunctional and structural changes were observed in the intestinal mucosal barrier in COPD model rats, which may be associated with the increased intestinal inflammatory responses.

No MeSH data available.


Related in: MedlinePlus