Biotechnology and Bioprocess Engineering 2019; 24(3): 445-453  
Pulmonary Protective Functions of Rare Ginsenoside Rg4 on Particulate Matter-induced Inflammatory Responses
Wonhwa Lee1,2,†, Sae-Kwang Ku3,†, Ji-Eun Kim4,†, Ga-Eun Choi4, Gyu-Yong Song4,*, and Jong-Sup Bae2,*
1Aging Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Deajeon 34141, Korea
2College of Pharmacy, CMRI, Research Institute of Pharmaceutical Sciences, BK21 Plus KNU Multi-Omics based Creative Drug Research Team, Kyungpook National University, Daegu 41566, Korea
3Department of Histology and Anatomy, College of Korean Medicine, Daegu Haany University, Gyeongsan 38610, Korea
4College of Pharmacy, Chungnam National University, Daejon 34134, Korea
Correspondence to: Jong-Sup Bae
Tel: +82-53-950-8570; Fax: +82-53-950-8557

Gyu-Yong Song
Tel: +82-42-821-5926; Fax: +82-42-823-6566

First three authors contributed equally to this work.
Received: March 18, 2019; Revised: March 20, 2019; Accepted: March 20, 2019; Published online: June 30, 2019.
© The Korean Society for Biotechnology and Bioengineering. All rights reserved.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Inhalation of fine particulate matter (PM2.5) is associated with an increase in lung injury caused by the loss of integrity of the vascular barrier. The rare ginsenoside Rg4 is a main protopanaxatriol type ginsenoside of black ginseng (BG). The aim of this study was to investigate the beneficial effects of Rg4 on 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 EC and mice. Rg4 significantly scavenged PM2.5-induced ROS, inhibited ROS-induced activation of p38 mitogen-activated protein kinase (MAPK), activated Akt in purified pulmonary endothelial cells, which helped maintain endothelial integrity. Further, Rg4 reduced vascular protein leakage, leukocyte infiltration, and proinflammatory cytokine release in bronchoalveolar lavage fluids in PM-induced mouse lung tissues. Data suggested that Rg4 might exhibit protective effects in PM-induced inflammatory lung injury and vascular hyperpermeability.
Keywords: Rg4, particulate matter, vascular permeability, Akt

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