| Objective:With living standards improved, living rhythm accelerated and working pressure enlarged, the consumption of alcohol and the number of alcoholics increases year by year. A WHO 2006 year's report demonstrats there is a causal relationship between alcohol consumption and more than 60 types of disease and injury. Alcohol on human beings has potential biological effects in almost every organ system. Drinking alcohol can lead to pregnant women and newborn diseases, cancer, neuropsychiatry diseases, cardiovascular diseases, cirrhosis, lung injury, accidental injury, and so on. The impact of alcohol on the lung have a great clinical importance, its volatility makes airway epithelium on high density ethanol surroundings. It can cause airway epithelial injury and lung tissue remodeling, and lead to alcohol-related pulmonary disease. At present, the research about alcohol-induced pulmonary fibrosis is little, so the study aims to set up the model of chronic ethanol ingestion induced pulmonary fibrosis in rats, and observe the effects of alcohol intake on lung tissue in glutathione, hydroxyproline content and CTGF, TIMP-1 expression to explore the relationship between alcohol and pulmonary fibrosis and it's possible mechanism for the pathogenesis of pulmonary fibrosis. It is significant to find the incidence of pulmonary fibrosis, at the same time to have further understanding the harm of chronic alcohol ingestion.Methods:According to the prescription of Lieber-DeCarli liquid diet, the isocaloric animal feed, which contained ethanol (36% total calories) or non-ethanol (substitution of Maltose-Dextrin for EtOH) was prepared. Clean healthy male Sprague-Dawley rats 20, weighing 160-200g, were randomly divided into control group (C group) 10 and alcohol group (A group) 10, and fed quantitative non-ethanol or ethanol Lieber-DeCarli liquid diet every day in a single cage for 8 weeks. As study completed, animals were sacrificed, thoracotomy complete separation of the trachea and lung tissue. By hematoxylin-eosin staining the morphological changes of lung tissue were observed, by Masson staining interstitial lung collagen deposition were observed; through colorimetric glutathione and hydroxyproline in lung tissue were measured; through Elisa CTGF,TIMP-l's expression of lung tissue were detected. SPSS15.0 statistical software was used for data processing, parameter data to mean±standard deviation. The level of significance was set as P< 0.05.Results:1.The general status:before the experiment the general condition of rats was normal eating, smooth glossy fur. There is no significant differences after the experiment food intake of rats in each group.The alcohol group's body weight grow slowly, gloomy fur, slowly moved, soft row of faceless stool.2. HE staining showed: the control group alveolar structure was clear, and alveolar walls interstitial have not inflammatory cell infiltrations. Alcohol group can be seen varying degrees of alveolar and alveolar septal infiltration of inflammatory cells, some alveolar wall damaged or collapsed. Masson results show:the experimental group had more deposition of collagen fibers at intervals of alveolar than the control group.3. Compared to the group C, the content of glutathione (GSH) in rat lung tissue reduced but hydroxyproline (HYP) increased in group A,the differences were statistically significant (P<0.05).4. CTGF and TIMP-1 in rat lung tissue of group A were higher than group C, the differences were statistically significant(P<0.05).Conclusion:This experiment proved Lieber-DeCarli Ethanol liquid diet can establish chronic ethanol ingestion rats'animal model. Alcohol can cause the reduction of glutathione in lung tissue, induce oxidized stress response; Oxidized stress products make rat lung tissue CTGF and TIMP-1 expression increase. And the lung tissue content of hydroxyproline increased. It was proved that alcohol play an important role on the formation of pulmonary fibrosis, suggesting that chronic ethanol ingestion can cause lung injury in rats, leading to pulmonary fibrosis.Alcohol may be one of the causes of pulmonary fibrosis.
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