Shuang-Huang-Lian exerts anti-inflammatory and anti-oxidative activities in lipopolysaccharide-stimulated murine alveolar macrophages

被引：59

作者：

Gao, Yuan ^{[1
,2
]}

Fang, Lei ^{[1
,2
]}

Cai, Runlan ^{[1
,2
]}

Zong, Chuanjie ^{[1
,2
,3
]}

Chen, Xi ^{[1
,2
]}

Lu, Juan ^{[1
,2
]}

Qi, Yun ^{[1
,2
]}

机构：

[1] Chinese Acad Med Sci, Inst Med Plant Dev, Beijing 100193, Peoples R China

[2] Peking Union Med Coll, Beijing 100193, Peoples R China

[3] Heilongjiang Univ Chinese Med, Harbin 150040, Peoples R China

来源：

PHYTOMEDICINE | 2014年 / 21卷 / 04期

基金：

中国国家自然科学基金;

关键词：

Shuang-Huang-Lian (SHL); Anti-inflammatory; Anti-oxidative; Murine alveolar macrophages (MH-S); AP-1; pathway; FACTOR-KAPPA-B; INFLAMMATORY MEDIATORS; CHLOROGENIC ACID; IN-VIVO; ACTIVATION; PATHWAY; EXTRACT; INJURY; ASSAY; BETA;

D O I：

10.1016/j.phymed.2013.09.022

中图分类号：

Q94 [植物学];

学科分类号：

071001 [植物学];

摘要：

Shuang-Huang-Lian (SHL) is a traditional Chinese compound formula prepared from Lonicerae Japonicae Flos, Scutellariae Radix and Fructus Forsythiae. In this study, we demonstrate the anti-inflammatory and anti-oxidative activities of SHL in lipopolysaccharide (LPS)-stimulated murine alveolar macrophages (MH-S). SHL significantly reduces the transcriptional and translational levels of iNOS and COX-2 as well as the production of NO and prostaglandin E-2 (PGE2). It also suppresses the transcription and translation of inflammatory cytokines production, such as TNF-a, IL-10 and IL-6. These inhibitory effects mainly act via ERK1/2- and p38-mediated AP-1 rather than the NF-KB pathway. In parallel with the antiinflammatory activity, SHL suppresses LPS-induced intracellular total ROS levels by weakening NADPH oxidase activity, enhancing SOD activity and increasing GSH content. In addition, SHL directly scavenges "OH and 02 Thus, our study elucidates the anti-inflammatory and anti-oxidative mechanisms of SHL in LPS-stimulated MR-S. (C) 2013 Elsevier GmbH. All rights reserved.

引用

页码：461 / 469

页数：9

共 29 条

[1]

Baicalin attenuates global cerebral ischemia/reperfusion injury in gerbils via anti-oxidative and anti-apoptotic pathways [J].