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胃酸和胃蛋白酶在模拟胃酸吸入导致大鼠肺纤维化中的协同作用。

Gastric Acid and Pepsin Work Together in Simulated Gastric Acid Inhalation Leading to Pulmonary Fibrosis in Rats.

机构信息

Department of Respiratory Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing, Jiangsu, China (mainland).

Department of Gastroenterology, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing, Jiangsu, China (mainland).

出版信息

Med Sci Monit. 2019 Aug 16;25:6153-6164. doi: 10.12659/MSM.915628.

Abstract

BACKGROUND The clinical association between gastroesophageal reflux disease (GERD) and idiopathic pulmonary fibrosis (IPF) has been known for many years, but it is still unclear. The present study investigated the association between experimentally simulated aspiration and pulmonary fibrosis. MATERIAL AND METHODS A total of 120 male Sprague-Dawley rats were randomly divided into a negative control group, a bleomycin group, and 3 simulated aspiration groups. The bleomycin group was administered a one-time intratracheal injection of bleomycin, whereas the 3 simulated aspiration groups were treated either with an intratracheal instillation of gastric fluid combined with pepsin, with pepsin alone, or with hydrochloric acid, all twice a week, and the negative control group was administered normal saline twice a week. Lung tissues were collected to evaluate pathological changes and the mRNA expression levels of connective tissue growth factor (CTGF), type I collagen, and transforming growth factor. RESULTS The results demonstrated that the degree of fibrosis in the early stage was low in each of the 3 simulated aspiration groups, but gradually increased over time. The expression levels of the downstream factor of fibrosis, CTGF, and type I collagen also reflected this trend. CONCLUSIONS The study demonstrates that aspiration of gastric contents can cause pulmonary fibrosis, and mixed aspiration of pepsin and gastric fluid can accelerate this process. This study provides strong evidence in support of a potential association between human GERD and IPF.

摘要

背景

胃食管反流病(GERD)和特发性肺纤维化(IPF)之间的临床关联已为人所知多年,但仍不清楚。本研究调查了实验模拟吸入与肺纤维化之间的关联。

材料和方法

将 120 只雄性 Sprague-Dawley 大鼠随机分为阴性对照组、博来霉素组和 3 个模拟吸入组。博来霉素组一次性气管内注射博来霉素,而 3 个模拟吸入组分别用胃蛋白酶、胃蛋白酶或盐酸进行气管内滴注,每周两次,阴性对照组每周两次给予生理盐水。收集肺组织评估病理变化和结缔组织生长因子(CTGF)、I 型胶原和转化生长因子的 mRNA 表达水平。

结果

结果表明,在每个模拟吸入组中,早期纤维化程度较低,但随着时间的推移逐渐增加。纤维化下游因子 CTGF 和 I 型胶原的表达水平也反映了这一趋势。

结论

本研究表明,胃内容物的吸入可导致肺纤维化,而胃蛋白酶和胃液的混合吸入可加速这一过程。本研究为 GERD 和 IPF 之间可能存在关联提供了有力证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3d7/6708284/3fd5c2b4c77d/medscimonit-25-6153-g001.jpg

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