求文献一篇。谢谢。

kouke80

Eur Respir J. 2013 Aug;42(2):350-61. doi: 10.1183/09031936.00042512. Epub 2012 Nov 22.
* r1 E* R2 i* |" ~; i1 uSimvastatin inhibits smoke-induced airway epithelial injury: implications for COPD therapy.8 `2 D; F( S& Y) c4 Z  ^9 g5 P4 H
Davis BB1, Zeki AA, Bratt JM, Wang L, Filosto S, Walby WF, Kenyon NJ, Goldkorn T, Schelegle ES, Pinkerton KE.$ A2 f& S) {/ I3 n0 |) Y- J
Author information+ x; x4 |+ e# I: b( e
Abstract
4 k% c0 t7 A+ d/ t/ ^/ I: _Chronic obstructive pulmonary disease (COPD) is the third leading cause of death. The statin drugs may have therapeutic potential in respiratory diseases such as COPD, but whether they prevent bronchial epithelial injury is unknown. We hypothesised that simvastatin attenuates acute tobacco smoke-induced neutrophilic lung inflammation and airway epithelial injury. Spontaneously hypertensive rats were given simvastatin (20 mg·kg(-1) i.p.) daily for either 7 days prior to tobacco smoke exposure and during 3 days of smoke exposure, or only during tobacco smoke exposure. Pretreatment with simvastatin prior to and continued throughout smoke exposure reduced the total influx of leukocytes, neutrophils and macrophages into the lung and airways. Simvastatin attenuated tobacco smoke-induced cellular infiltration into lung parenchymal and airway subepithelial and interstitial spaces. 1 week of simvastatin pretreatment almost completely prevented smoke-induced denudation of the airway epithelial layer, while simvastatin given only concurrently with the smoke exposure had no effect. Simvastatin may be a novel adjunctive therapy for smoke-induced lung diseases, such as COPD. Given the need for statin pretreatment there may be a critical process of conditioning that is necessary for statins' anti-inflammatory effects. Future work is needed to elucidate the mechanisms of this statin protective effect.1 K! Z- y9 z/ s* J% ]7 @% X
PMID: 23180589 [PubMed - indexed for MEDLINE]
9 c3 I( B* s9 r3 E: ~3 N7 M9 \# K& q7 C9 A8 l1 `

kouke80

已解决谢谢。2 A. C7 B- L. {