中文摘要：

在在航线上皮的呼吸的道和离脚玻璃杯或瓷杯房间组织变形的背景粘液分泌过盛贡献与煽动性的 diseases.This 学习试图在与 lipopolysaccharide ( LPS )对待的老鼠在航线粘液分泌过盛上检验 simvastatin 的效果和机制的航线联系的病态和死亡在老鼠航线的 .Methods 粘液分泌过盛被导致被对待与或没有 LPS 的 LPS.Rats 的intra气管的灌输 intra-peritoneally 管理 simva

英文摘要：

Background Mucus hypersecretion in the respiratory tract and goblet cell metaplasia in the airway epithelium contribute to the morbidity and mortality associated with airway inflammatory diseases. This study aimed to examine the effect and mechanisms of simvastatin on airway mucus hypersecretion in rats treated with lipopolysaccharide （LPS）. Methods Mucus hypersecretion in rat airways was induced by intra-tracheal instillation of LPS. Rats treated with or without LPS were administered intra-peritoneally simvastatin （5 and 20 mg/kg） for 4 days. Expression of Muc5ac, RhoA and mitogen-activated protein kinases （MAPK） p38 in lung were detected by real-time polymerase chain reaction （PCR）, immunohistochemistry or Western blotting. Tumor necrosis factor （TNF）-α and IL-8 in bronchoalveolar lavage fluid （BALF） were assayed by an enzyme-linked lectin assay and enzyme linked immunosorbent assay （ELISA）. Results Simvastatin attenuated LPS-induced goblet cell hyperplasia in bronchial epithelium and Muc5ac hypersecretion at both the gene and protein levels in lung （P 〈0.05）. Moreover, simvastatin inhibited neutrophil accumulation and the increased concentration of TNF-α and IL-8 in BALF follows LPS stimulation （P 〈0.05）. The higher dose of simvastatin was associated with a more significant reduction in Muc5ac mRNA expression, neutrophil accumulation and inflammatory cytokine release. Simultaneously, the increased expression of RhoA and p38 MAPK were observed in LPS-treated lung （P 〈0.05）. Simvastatin inhibited the expression of RhoA and p38 phosphorylation in lung following LPS stimulation （P 〈0.05）. However, the increased expression of p38 protein in LPS-treated lung was not affected by simvastatin administration. Conclusions Simvastatin attenuates airway mucus hypersecretion and pulmonary inflammatory damage induced by LPS. The inhibitory effect of simvastatin on airway mucus hypersecretion may be through, at least in part, the suppression of neutrophil accumulation and