Inhibitory Effects of Black Ginseng on Particulate Matter-Induced Pulmonary Injury

被引:28
作者
Lee, Wonhwa [1 ,2 ]
Ku, Sae-Kwang [3 ]
Kim, Ji-Eun [4 ]
Cho, Soo-Hyun [4 ]
Song, Gyu-Yong [4 ]
Bae, Jong-Sup [2 ]
机构
[1] Korea Res Inst Biosci & Biotechnol, Aging Res Ctr, Deajeon 34141, South Korea
[2] Kyungpook Natl Univ, BK21 Plus KNU Multiom Based Creat Drug Res Team, Res Inst Pharmaceut Sci, Coll Pharm,CMRI, Daegu 41566, South Korea
[3] Daegu Haany Univ, Coll Korean Med, Dept Histol & Anat, Gyongsan 38610, South Korea
[4] Chungnam Natl Univ, Coll Pharm, 99 Daehak Ro, Daejon 34134, South Korea
来源
AMERICAN JOURNAL OF CHINESE MEDICINE | 2019年 / 47卷 / 06期
基金
新加坡国家研究基金会;
关键词
Black Ginseng Extract; Particulate Matter; Vascular Permeability; Akt; AIR-POLLUTION; OXIDATIVE STRESS; PANAX-GINSENG; LUNG INJURY; CELL-LINE; PM2.5; RG5; HYPERRESPONSIVENESS; GINSENOSIDES; INFLAMMATION;
D O I
10.1142/S0192415X19500630
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
Inhalation of fine particulate matter (PM2.5) is associated with elevated pulmonary injury caused by the loss of vascular barrier integrity. Black ginseng (BG), steamed and dried ginseng nine times, exhibits various pharmacological activities such as antibacterial, anti-hyperglycemic, anti-atopic, antibacterial, and anti-inflammatory activities. In this study, we investigated the beneficial effects of black ginseng extract (BGE) against PM-induced lung endothelial cell (EC) barrier disruption and pulmonary inflammation. Permeability, leukocyte migration, activation of proinflammatory proteins, generation of reactive oxygen species (ROS), and histology were examined in PM2.5-treated ECs and mice. BGE significantly scavenged PM2.5-induced ROS and inhibited the ROS-induced activation of p38 mitogen-activated protein kinase (MAPK). Concurrently, BGE activated Akt, which helped maintain endothelial integrity. Furthermore, BGE reduced vascular protein leakage, leukocyte infiltration, and proinflammatory cytokine release in the bronchoalveolar lavage fluid in PM-induced lung tissues. These results indicated that BGE may exhibit protective effects against PM-induced inflammatory lung injury and vascular hyperpermeability.
引用
收藏
页码:1237 / 1251
页数:15
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