论文部分内容阅读
目的观察培哚普利对慢性阻塞性肺疾病(简称慢阻肺)大鼠肺功能及肺组织磷酯酰肌醇3-激酶(PI3K)的影响,为培哚普利治疗慢阻肺提供科学依据。方法将60只雄性SD大鼠随机分为正常对照组、模型组及培哚普利干预组,每组各20只。采用两次气管滴注脂多糖(LPS)加烟熏的方法建立慢阻肺大鼠模型,第28 d时检测大鼠肺功能和肺组织中PI3K表达水平,HE染色观察大鼠肺组织病理改变。结果模型组大鼠肺组织HE染色符合慢阻肺的病理改变,培哚普利干预组肺气肿程度较慢阻肺组大鼠减轻;模型组、干预组大鼠的肺功能与对照组比较均有下降,模型组的每分钟呼气量(VE)、最大呼气流量(PEP)和0.3 s用力呼气容积(FEV0.3)较干预组下降更为显著,差异均有统计学意义(P<0.01或P<0.05);模型组、干预组肺组织中PI3K表达水平与对照组比较均有上升,差异均有统计学意义(P<0.01或P<0.05),但模型组较干预组上升更为显著,差异均有统计学意义(P<0.05)。结论培哚普利能明显改善慢阻肺大鼠肺功能,其机制可能是通过下调肺组织中PI3K的表达水平来实现的。
Objective To observe the effect of perindopril on pulmonary function and pulmonary phosphatidylinositol 3-kinase (PI3K) in rats with chronic obstructive pulmonary disease (COPD), and to provide a scientific basis for perindopril in treating chronic obstructive pulmonary disease in accordance with. Methods Sixty male SD rats were randomly divided into normal control group, model group and perindopril intervention group, with 20 rats in each group. The model of chronic obstructive pulmonary disease was established by tracheal instillation of lipopolysaccharide (LPS) plus smoked method. The lung function and the expression of PI3K in lung tissue were detected on the 28th day. The pathological changes of the lung tissue were observed by HE staining . Results The lung tissue of rats in the model group was consistent with the pathological changes of COPD. The rats in the perindopril group had lower degree of emphysema than the COPD group. The pulmonary function of the model group and the intervention group was significantly lower than that of the control group (VE), maximum expiratory flow (PEP) and forced expiratory volume at 0.3 s (FEV0.3) in the model group were significantly lower than those in the intervention group (P <0.05), and the differences were statistically significant P <0.01 or P <0.05). Compared with the control group, the expression of PI3K in the model group and the intervention group both increased, the differences were statistically significant (P <0.01 or P <0.05) Rise more significantly, the differences were statistically significant (P <0.05). Conclusion Perindopril can significantly improve lung function in COPD rats, and its mechanism may be through down-regulating the expression of PI3K in lung tissue.