Abstract:

Objective   To determine the effect and mechanism of simvastatin on lung apoptotic factors in chronic obstructive pulmonary disease(COPD)rat models. Methods   30 rats were randomly divided into three groups: the normal group, the control group and the treatment group. The control group was treated by being exposed to smoking and intratracheal instillation of lipopolysaccharide to establish the COPD rat models. 2 weeks later, the treatment group was treated with 2.5mg/kg simvastatin daily for 6 weeks. The rats were executed after 8 weeks. Lung tissue sections stained by hematoxylin and eosin (HE) were observed, and mean linear intercept as well as mean alveolar numbers were measured by micrographical analysis. Expressions of eNOS, iNOS and caspase-3 were measured by immunohistochemistry. Results   Emphysema and airway inflammation were observed in the control group, and the symptoms of the treatment group were lighter. Compared with the normal group, the mean linear intercept(MLI), iNOS, Caspase-3 in the control and treatment groups increased(P<0.05), and the mean alveolar numbers (MAN) and eNOS decreased(P<0.05). Compared with the control group, the MLI, iNOS, Caspase-3 decreased(P<0.05) and the MAN and eNOS increased(P<0.05) in the treatment group. Caspase-3 in the lung tissue of each group positively correlated with iNOS(P<0.05), and negatively with eNOS(P<0.05). Conclusion   Simvastatin has a protective effect on the COPD rat models by increasing expression of eNOS and decreasing the expressions of iNOS and Caspase-3 which can reduce the apoptosis of COPD lung tissue.

Key words: Pulmonary disease, chronic obstructive; Apoptosis; Simvastatin; Rats