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Journal of Anesthesiology and Pain Research

ISSN: 2684-5997

Open Access

Effect of Atorvastatin on Lung Apoptosis-Associated Protein Caspase-12 in Chronic Obstructive Pulmonary Disease (COPD) Model Rats

Abstract

Li-Le Wang , Chun-Chu Kong , Yun-Rong Chen, Dai-Yan Fu, Jie Li, Chang-Yu Huang, Gui-Xiang Gan, Bin-Bin Chen, Mo Liang, Ming Xu, Rui-Cheng Hu1, Shuang-Xiang Tan and Ai-guo Dai

Abstract
Objective: To determine the effect of atorvastatin on the expression of lung apoptosis-associated protein caspase-12 in Chronic Obstructive Pulmonary Disease (COPD) model rats.
Methods: 30 rats were randomly divided into three groups: the normal group, the control group, and the treatment group. The control group and the treatment group were treated by being exposed to smoking and intratracheal instillation of lipopolysaccharide to establish the COPD model rats. 2 weeks later, the treatment group was treated with 2.5 mg/kg atorvastatin daily for 6 weeks. Nothing was done in the normal group. The rats were executed after 8 weeks. Lung tissue sections stained by Hematoxylin and Eosin (HE) were observed. The protein and gene expression of lung apoptosis-associated caspase-12 in each group was investigated by RT-PCR and immunohistochemistry.
Results: Pulmonary histopathology: emphysema and airway inflammation were observed in the control group, and the symptoms of the treatment group were lighter. RT-PCR: compared with the normal group, a higher level of caspase-12 mRNA was expressed in the control group and the treatment group (p<0.05); compared with the control group, lower level of caspase-12 mRNA was expressed in the treatment group (p<0.05). Immunohistochemistry: compared with the normal group, the expression of caspase-12 increased in the control group and the treatment group (p<0.05). Compared with the control group, the expression of caspase-12 decreased (p<0.05).
Conclusion: Atorvastatin has a protective effect on the COPD model rats by decreasing the protein and gene expression of caspase-12 which can reduce the apoptosis of COPD lung tissue.

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