红霉素对被动吸烟大鼠肺组织气肿样变的保护作用

目的观察红霉素对被动吸烟大鼠肺组织气肿样变的保护作用并初步探讨其作用机制。方法 40只SD大鼠随机分为正常对照组、模型组、红霉素组、桂龙咳喘宁对照组,每组10只;采用气管内注入脂多糖(LPS)及烟熏的混合刺激方法建立肺气肿大鼠模型,造模3周后进行药物干预,连续14 d。肺组织病理切片观察形态学改变并采用图像分析系统检测平均肺泡面积(MAA),平均肺泡数(MAN)和肺平均内衬间隔(MLI),免疫组化测定肺组织中MMP-2与TIMP-2的表达量,ELISA法测定血清中IL-10与TNF-α的浓度。结果模型组大鼠肺组织可见肺大泡形成,MAA明显增大,MAN明显减少以及MLI显著增大,且有明显的炎症细胞浸润以及血清中TNF-α的浓度明显升高,与正常组比较有显著性差异(P<0.05);红霉素组(100 mg.kg?1)未见肺大泡形成,炎症细胞浸润明显减轻,且能明显降低肺组织中MMP-2表达量与血清中TNF-α的浓度,并能明显的增加肺组织中TIMP-2的表达量与血清中IL-10的浓度,与模型组比较有显著性差异(P<0.05),与桂龙咳喘宁组(450 mg.kg?1)相比无显著性的差异。结论红霉素对被动吸烟大鼠肺组织气肿样变具有明显的保护作用。

Protective Effect of Erythromycin on Cigarette-induced Emphysema in Rats

OBJECTIVE To observe the protective effect of erythromycin on cigarette-induced emphysema in rats and preliminarily discuss its mechanism.METHODS Forty SD rats were randomly divided into control group,cigarette-induced emphysema group,Erythromycin pill group,Guilong Kechuanning group.Rat model of emphysema was established by intratracheal instillation of lipopolysaccharide（LPS） twice and exposed to cigarette smoke daily.After 3 weeks,the rats were administrated by gastric lavage of corresponding drugs for 14 d.Pathological changes of the lungs were observed and MAA,MAN and MLI were measured by image analysis system.Immunohistochemical determined the expression of MMP-2 and TIMP-2 in lung tissue.The expression of IL-10 and TNF-α was examined by ELISA.RESULTS Compared with the control group,pathological changes with obvious emphysema and inflammation cell infiltrates were found after modeling.MAA and MLI increased significantly,MAN obviously decreased,and the expression of TNF-α in serum increased significantly（P0.05）.Erythromycin（100 mg·kg 1） could obviously lessen the formation of emphysema and the infiltrations of inflammatory cells,reduce the expression of MMP-2 in lung tissue and TNF-in serum,and increase the expression of TIMP-2 in lung tissue and IL-10 in serum（P0.05）.There was no difference between erythromycin group and Guilong Kechuanning group.CONCLUSION Erythromycin pill had significantly protective effect on cigarette-induced emphysema in rats.