Pathological characteristics of digestive tract in rats with chronic obstructive pulmonary disease induced by tobacco smoke

Difei Li, Defu Li, Zeguang Zheng, Wenju Lu, Jieying Hu, Rongchang Chen
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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
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烟草烟雾致慢性阻塞性肺疾病大鼠消化道病理特征
目的观察慢性阻塞性肺疾病(COPD)大鼠消化道的病理变化,为探讨COPD营养不良的发生机制提供理论依据。方法建立慢性阻塞性肺病大鼠香烟烟雾暴露模型。采用Buxco肺功能测量系统测定肺功能。采用GEM3000血气分析仪检测动脉血气参数。计数炎性细胞,酶联免疫吸附法检测支气管肺泡灌洗液(BALF)中白细胞介素-6 (IL-6)、单核细胞化学引诱蛋白-1 (MCP-1)和白细胞介素-10水平。观察肺、肝、脾、胃、小肠的病理变化。结果造模结束时,模型组大鼠体重明显低于对照组。与对照大鼠相比,CS暴露大鼠呈现典型的copd样肺功能下降,表现为功能残气量(FRC)、总肺活量(TLC)、Chord顺应性(Cchord)升高,FEV50/FVC比值降低。暴露于CS的大鼠肺中可见肺泡壁和肺大泡的损伤。肺泡灌洗液中炎症细胞总数、中性粒细胞、巨噬细胞和淋巴细胞的分类计数以及促炎介质IL-6和MCP-1的水平均高于对照组。抗炎细胞因子IL-10低于对照组。组织学染色显示肝中央小叶轻度充血伴炎性细胞浸润,轻度肝水肿,脾脏少量充血,胃轻度糜烂,小肠黏膜萎缩伴少量炎性细胞浸润。结论慢性阻塞性肺病患者消化道组织包括肝、脾、胃黏膜、小肠黏膜均出现充血、水肿、充血、糜烂、炎症细胞浸润等胃肠道病理改变。关键词:肺部疾病;慢性阻塞性肺疾病;炎症;消化道的病理改变
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