中国药房Issue(4)：464-467,4.DOI:10.6039/j.issn.1001-0408.2016.04.10
3-甲基嘌呤对脂多糖诱导小鼠急性肺损伤的保护作用及其机制研究
Protective Effects of 3-Methyladenine against Lipopolysaccharide-induced Acute Lung Injury in Mice and the Mechanism Study
摘要
Abstract
OBJECTIVE:To study the protective effects of autophagy inhibitor 3-Methyladenine (3-MA) against lipopolysac-charide(LPS)-induced acute lung injury in mice and its mechanism. METHODS:Mice were randomly divided into normal control group,model group (LPS 15 mg/kg),drug control group (3-MA 20 mg/kg),low-dose and high-dose groups (LPS 15 mg/kg+3-MA 20,40 mg/kg),with 10 mice in each group. Except for normal control group and drug control group,other groups were giv-en LPS intraperitoneally to induce acute lung injury model,and drug control group and low-dose and high-dose groups were given equivalent dose of 3-MA intraperitoneally 1 h before modeling. 6 h after modeling,lung wet/drug mass ratio (W/D) was deter-mined respectively,and pathology change of lung tissue was observed by HE staining. TNF-α,NF-κB p65,LC3BⅡ/Ⅰ and Cleaved-caspase-3 protein expression were detected by Western blot. RESULTS:Compared with normal control group,W/D, TNF-α,NF-κB p65,LC3BⅡ/Ⅰ and Cleaved-caspase-3 protein expression increased in model group (P<0.01). Compared with model group,W/D,the expression of TNF-α,NF-κB p65,LC3BⅡ/Ⅰ and Cleaved-caspase-3 protein decreased in low-dose group (P<0.05),white just only LC3BⅡ/Ⅰ protein decreased high-dose group(P<0.01). CONCLUSIONS:In LPS-induced acute lung injury model in mice,the excessive autophagy could activate the NF-κB pathway and involve the inflammatory responses and induce lung cells apoptosis. The moderate autophagy inhibition by 3-MA can ameliorate inflammatory response and protect lung tissue.关键词
自噬/3-甲基嘌呤/急性肺损伤/脂多糖/小鼠Key words
Autophagy/3-Methyladenine/Acute lung injury/Lipopolysaccharide/Mice分类
医药卫生引用本文复制引用
朱贲贲,马晓鹂,吴科锋,陈华玲..3-甲基嘌呤对脂多糖诱导小鼠急性肺损伤的保护作用及其机制研究[J].中国药房,2016,(4):464-467,4.基金项目
广东省自然科学基金自由申请重点博士启动项目 （）
