{"title":"Pathological characteristics of digestive tract in rats with chronic obstructive pulmonary disease induced by tobacco smoke","authors":"Difei Li, Defu Li, Zeguang Zheng, Wenju Lu, Jieying Hu, Rongchang Chen","doi":"10.3760/CMA.J.ISSN.1673-436X.2020.05.001","DOIUrl":null,"url":null,"abstract":"Objective \nTo observe the pathological changes of the digestive tract of rats with chronic obstructive pulmonary disease (COPD), as well as to provide a theoretical basis for exploring the mechanism of COPD dystrophy. \n \n \nMethods \nThe COPD rat model was established by cigarette smoke (CS) exposure.Lung functions were measured using Buxco lung function measurement system.Arterial blood gas parameters were examined with GEM3000 blood gas analyzer.The inflammatory cells were counted and the level of interlukin-6 (IL-6), monocyte chemo-attractant protein-1 (MCP-1) and IL-10 in bronchoalveolar lavage fluid (BALF) were assayed with enzyme-linked immunosorbent assay.Pathological changes of lung tissue, liver, spleen, stomach, small intestine were observed. \n \n \nResults \nAt the end of modeling, the weight of the model group rats were significantly lower than those of the control group.Compared with control rats, the CS exposed rats presented typical COPD-like lung function decline indicated by increases in functional residual volume (FRC), total lung capacity (TLC), Chord compliance (Cchord), as well as a decrease in the FEV50/FVC ratio.Damaged alveolar walls and pulmonary bullae were observed in rats′ lungs exposed to CS.In alveolar lavage fluid, the total number of inflammatory cells and the categorical counts (neutrophils, macrophages, and lymphocytes) were higher than those of the control group, as well as the levels of IL-6 and MCP-1 as proinflammatory mediators.The anti-inflammatory cytokine IL-10 was lower than that of the control group.Moreover, the histological staining showed that a little congestion in the central hepatic lobule with inflammatory cell infiltration and mild hepatic edema, a small amount of congestion in the spleen, mild erosion in the stomach, small intestine mucosal atrophy with a small amount of inflammatory cell infiltration. \n \n \nConclusions \nIn COPD, gastrointestinal pathological changes including hyperemia, edema, congestion, erosion, and inflammatory cell infiltration are observed in the digestive tract tissues including liver, spleen, gastric mucosa, and small intestinal mucosa. \n \n \nKey words: \nPulmonary disease, chronic obstructive; Inflammation; Pathological changes in the digestive tract","PeriodicalId":10004,"journal":{"name":"Chinese Journal of Asthma","volume":"387 1","pages":"321-326"},"PeriodicalIF":0.0000,"publicationDate":"2020-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Chinese Journal of Asthma","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3760/CMA.J.ISSN.1673-436X.2020.05.001","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Objective
To observe the pathological changes of the digestive tract of rats with chronic obstructive pulmonary disease (COPD), as well as to provide a theoretical basis for exploring the mechanism of COPD dystrophy.
Methods
The COPD rat model was established by cigarette smoke (CS) exposure.Lung functions were measured using Buxco lung function measurement system.Arterial blood gas parameters were examined with GEM3000 blood gas analyzer.The inflammatory cells were counted and the level of interlukin-6 (IL-6), monocyte chemo-attractant protein-1 (MCP-1) and IL-10 in bronchoalveolar lavage fluid (BALF) were assayed with enzyme-linked immunosorbent assay.Pathological changes of lung tissue, liver, spleen, stomach, small intestine were observed.
Results
At the end of modeling, the weight of the model group rats were significantly lower than those of the control group.Compared with control rats, the CS exposed rats presented typical COPD-like lung function decline indicated by increases in functional residual volume (FRC), total lung capacity (TLC), Chord compliance (Cchord), as well as a decrease in the FEV50/FVC ratio.Damaged alveolar walls and pulmonary bullae were observed in rats′ lungs exposed to CS.In alveolar lavage fluid, the total number of inflammatory cells and the categorical counts (neutrophils, macrophages, and lymphocytes) were higher than those of the control group, as well as the levels of IL-6 and MCP-1 as proinflammatory mediators.The anti-inflammatory cytokine IL-10 was lower than that of the control group.Moreover, the histological staining showed that a little congestion in the central hepatic lobule with inflammatory cell infiltration and mild hepatic edema, a small amount of congestion in the spleen, mild erosion in the stomach, small intestine mucosal atrophy with a small amount of inflammatory cell infiltration.
Conclusions
In COPD, gastrointestinal pathological changes including hyperemia, edema, congestion, erosion, and inflammatory cell infiltration are observed in the digestive tract tissues including liver, spleen, gastric mucosa, and small intestinal mucosa.
Key words:
Pulmonary disease, chronic obstructive; Inflammation; Pathological changes in the digestive tract