Effects of Perindopril on Expression of PI3K and Lung Function in COPD Rats_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

WangJunpeng ,  BaoMingwei

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China;

Corresponding author：

BaoMingwei, Email: wjp7811@126.com

Keywords：

Chronic obstructive pulmonary disease; Perindopril; Phosphatidylinositol 3-kinase; Lipopolysaccharide

DOI：

10.7507/1671-6205.2015064

Video：

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Objective To observe the effects of perindopril on expression level of phosphatidylinositol 3-kinase (PI3K) and lung function in rats with obstructive pulmonary disease (COPD),and investigate the therapeutic effects of perindopril on COPD. Methods Sixty male SD rats were randomly divided into a control group,a COPD group,and a perindopril group,with 20 rats in each group. The rat model of COPD was established by intratracheal instillation of lipopolysachride and exprosure to cigarette smoke in the COPD group and the perindopril group. The rats in the perindopril group were intragastricly infused with perindopril additionally. All rats were sacrificed after 28 days. The lung function was observed and PI3K protein expression was detected using Western blot method. The pathologic changes of the lung tissue and airway were observed by HE staining. Results HE staining revealed that the rat COPD model was successfully established. The COPD group appeared obvious emphysema which was allievated significantly in the perindopril group. Pulmonary function indices in the COPD group and the perindopril group were significantly decreased compared with the control group with V_E value decreased by 40% and 22%,PEP value decreased by 33% and 15%,and FEV_0.3 value decreased by 18% and 7%,respectively. The expression of PI3K was significantly increased in the COPD group and the perindopril group than the control group,but more significantly in the COPD group (P<0.05). Conclusion Perindopril can significantly improve lung function in rats with COPD possibly through down-regulation of PI3K expression in the lung.

Citation： WangJunpeng, BaoMingwei. Effects of Perindopril on Expression of PI3K and Lung Function in COPD Rats. Chinese Journal of Respiratory and Critical Care Medicine, 2015, 14(3): 260-263. doi: 10.7507/1671-6205.2015064 Copy

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1. Song G,Ouyang GL,Bao SD. The activation of Akt/PKB signaling pathway and cell survival. J Cell Mol Med,2005,9:59-71.
2. Del Fiorentino A,Cianchetti S,Celi A,et al. The effect of angiotensin receptor blockers on C-reactive protein and other circulating inflammatory indices in man. Vasc Health Risk Manag,2009,5:233-242.
3. Liu L,Qiu HB,Yang Y,et al. Losartan,an antagonist of AT1 receptor for angiotensin Ⅱ,attenuates lipopolysaccharide-induced acute lung injury in rat. Arch Biochem Biophys,2009,481:131-136.
4. 沈利汉,莫红缨,蔡立华,等.肾素-血管紧张素系统与ALI/ARDS的关系探讨.中国呼吸与危重监护杂志,2010,9:310-314.
5. 宋一平,崔德健,茅培英.慢性阻塞性肺疾病大鼠模型的建立及药物干预的影响.中华内科杂志,2000,39:556-557.
6. Rameh LE,Cantley LC. The role of phosphoinositide 3-kinase lipid products in cell function. J Biol Chem,1999,274:8347-8350.
7. Stein RC,Waterfield MD. PI3-kinase inhibition:a target for drug development? Mol Med Today,2000,6:347-357.
8. 刘瑾,陈俊文,徐永健,等.磷脂酰肌醇3激酶在支气管哮喘大鼠气道平滑肌细胞中的表达.中国病理生理杂志,2008,24:636-639.
9. Larocca NE,Moreno D,Garmendia JV,et al. Inhibitors of phosphoinositol 3 kinase and NFkappaB for the treatment of chronic obstructive pulmonary disease. Recent Pat Inflamm Allergy Drug Discov,2011,5:178-183.
10. 方晓聪.磷酸肌醇3-激酶信号通路参与肺损伤修复及机制探讨.上海:复旦大学,2012,88-89.
11. Munshi MK,Uddin MN,Glaser SS. The role of the renin-angiotensin system in liver fibrosis. Exp Biol Med (Maywood),2011,236:557-566.
12. Uemura H,Ishiguro H,Ishiguro Y,et al. Angiotensin Ⅱ induces oxidative stress in prostate cancer. Mol Cancer Res,2008,6:250-258.
13. Liu JJ,Li DL,Zhou J,et al. Acetylcholine prevents angiotensin II-induced oxidative stress and apoptosis in H9c2 cells. Apoptosis,2011,16:94-103.

Chinese Journal of Respiratory and Critical Care Medicine

Effects of Perindopril on Expression of PI3K and Lung Function in COPD Rats

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