慢性饮酒引起大鼠肺组织损伤及肺纤维化

目的建立慢性饮酒大鼠模型,测定肺组织谷胱甘肽、羟脯氨酸和结缔组织生长因子（CTGF）含量,探讨酒精与肺纤维化的关系。方法 SD大鼠20只,随机分成酒精组和对照组。每日分别给予含和不含酒精的Lieber-DeCarli液体饲料单笼喂养,不再提供饮水。各组动物均于8周后处死,HE染色观察肺组织大体病理改变,Masson染色观察肺间质中胶原沉积情况,比色法检测肺组织中谷胱甘肽、羟脯氨酸的含量,ELISA测定肺组织中CTGF的含量。结果酒精组大鼠的肺泡及肺泡间隔有明显的炎性细胞浸润,部分肺泡壁破坏、塌陷,肺泡间隔中胶原纤维沉积增多、间隔增宽。酒精组大鼠肺组织匀浆羟脯氨酸和CTGF含量高于对照组,谷胱甘肽含量低于对照组羟脯氨酸：（0.57±0.15）mg/g比（0.40±0.09）mg/g;CTGF：（306.57±46.86）ng/mL比（134.02±79.82）ng/mL;谷胱甘肽：（0.08±0.04）mg/g比（0.22±0.14）mg/g;P均〈0.05]。结论用Lieber-DeCarli酒精液体饲料喂养可建立慢性饮酒大鼠模型。慢性饮酒可引起大鼠肺组织损伤和间质改变,酒精可能是引起肺纤维化的因素之一。

Chronic Ethanol Ingestion Induces Lung Injury and Pulmonary Fibrosis in Rats

Objective To explore the role of chronic ethanol ingestion in pulmonary fibrosis.Methods Twenty SD rats were randomly divided into a control group(n=10) and an ethanol group(n=10),and fed with quantitative non-ethanol and ethanol Lieber-DeCarli liquid diet every day respectively.All rats were sacrificed after 8 weeks.The morphological changes and collagen deposition of lung tissue were observed under light microscope by HE and Masson staining.Levels of glutathione(GSH) and hydroxyproline(HYP) in lung tissues were measured by colorimetric method.The content of connective tissue growth factor(CTGF) in lung tissue was detected by ELISA.Results Compared with the control group,varied degrees of alveolar and alveolar septal infiltration of inflammatory cells can be shown in the ethanol group,and also some alveolar wall damage or collapse.Masson staining showed that the ethanol group has more significant deposition of collagen fibers in alveolar interstitum than the control group.The content of GSH in rat lung tissue reduced,but the contents of HYP and CTGF increased in the ethanol group compared with the control group 0.09,CTGF(ng/mL):306.57±46.86 vs.134.02±79.82,P<0.05].Conclusions Lieber-DeCarli ethanol liquid diet can establish a rat model of chronic ethanol ingestion.Lung injury and pulmonary fibrosis in rats can be induced by chronic ethanol ingestion.Ethanol may be one of the causes of the pulmonary fibrosis.