Compound K ameliorates airway inflammation and mucus secretion through the regulation of PKC signaling in vitro and in vivo

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Title
Compound K ameliorates airway inflammation and mucus secretion through the regulation of PKC signaling in vitro and in vivo
Author(s)
Jae-Won LeeMun-Ock Kim; Yu Na Song; Jae-Hong Min; Seong Man Kim; Myung Ji Kang; Eun Sol Oh; Ro-Woon Lee; Sunin Jung; H Ro; J K Lee; Hyung Won Ryu; D Y Lee; Su Ui Lee
Bibliographic Citation
Journal of Ginseng Research, vol. 46, no. 3, pp. 496-504
Publication Year
2022
Abstract
Background: Cigarette smoke (CS) is considered a principal cause of chronic obstructive pulmonary disease (COPD) and is associated with mucus hypersecretion and airway inflammation. Ginsenoside compound K (CK), a product of ginsenoside metabolism, has various biological activities. Studies on the effects of CK for the treatment of COPD and mucus hypersecretion, including the underlying signaling mechanism, have not yet been conducted. Methods: To study the protective effects and molecular mechanism of CK, phorbol 12-myristate 13-acetate (PMA)-induced human airway epithelial (NCI?H292) cells were used as a cellular model of airway inflammation. An experimental mouse COPD model was also established via CS inhalation and intranasal administration of lipopolysaccharide. Mucin 5AC (MUC5AC), monocyte chemoattractant protein-1, tumor necrosis factor-α (TNF-α), and interleukin-6 secretion, as well as elastase activity and reactive oxygen species production, were determined through enzyme-linked immunosorbent assay. Inflammatory cell influx and mucus secretion in mouse lung tissues were estimated using hematoxylin and eosin and periodic acid?schiff staining, respectively. PKCδ and its downstream signaling molecules were analyzed via western blotting. Results: CK prevented the secretion of MUC5AC and TNF-α in PMA-stimulated NCI?H292 cells and exhibited a protective effect in COPD mice via the suppression of inflammatory mediators and mucus secretion. These effects were accompanied by an inactivation of PKCδ and related signaling in vitro and in vivo. Conclusion: CK suppressed pulmonary inflammation and mucus secretion in COPD mouse model through PKC regulation, highlighting the compound's potential as a useful adjuvant in the prevention and treatment of COPD.
Keyword
Lung inflammationCOPDGinsenoside compound KMUC5ACPKCd
ISSN
1226-8453
Publisher
Korea Soc-Assoc-Inst
DOI
http://dx.doi.org/10.1016/j.jgr.2021.12.008
Type
Article
Appears in Collections:
Ochang Branch Institute > Natural Product Research Center > 1. Journal Articles
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