Protective effect of Palmijihwanghwan in a mouse model of cigarette smoke and lipopolysaccharide-induced chronic obstructive pulmonary disease

Abstract Background Palmijihwanghwan (PJH) is a traditional medicine and eight constituents derived from PJH possess anti-inflammatory activities. However, the scientific evidence for its potential as a therapeutic agent for inflammatory lung disease has not yet been studied. In this study, we exami...

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Autores principales: Eun Bok Baek, Jin-hyung Rho, Eunhye Jung, Chang-Seob Seo, Jin-Hee Kim, Hyo-Jung Kwun
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Publicado: BMC 2021
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spelling oai:doaj.org-article:a877c825ec9e4be9b8141268eeb055392021-11-21T12:39:48ZProtective effect of Palmijihwanghwan in a mouse model of cigarette smoke and lipopolysaccharide-induced chronic obstructive pulmonary disease10.1186/s12906-021-03453-52662-7671https://doaj.org/article/a877c825ec9e4be9b8141268eeb055392021-11-01T00:00:00Zhttps://doi.org/10.1186/s12906-021-03453-5https://doaj.org/toc/2662-7671Abstract Background Palmijihwanghwan (PJH) is a traditional medicine and eight constituents derived from PJH possess anti-inflammatory activities. However, the scientific evidence for its potential as a therapeutic agent for inflammatory lung disease has not yet been studied. In this study, we examined the protective effect of PJH in a mouse model of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke (CS) with lipopolysaccharide (LPS). Methods Mice received CS exposure for 8 weeks and intranasal instillation of LPS on weeks 1, 3, 5 and 7. PJH (100 and 200 mg/kg) was administrated daily 1 h before CS treatment for the last 4 weeks. Results Compared with CS plus LPS-exposed mice, mice in the PJH-treated group showed significantly decreased inflammatory cells count and reduced inflammatory cytokines including interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor alpha (TNF-α) levels in broncho-alveolar lavage fluid (BALF) and lung tissue. PJH also suppressed the phosphorylation of nuclear factor kappa B (NF-κB) and extracellular signal-regulated kinase1/2 (ERK1/2) caused by CS plus LPS exposure. Furthermore, CS plus LPS induced increases in matrix metallopeptidase (MMP)-7, MMP-9, and transforming growth factor-β (TGF-β) expression and collagen deposition that were inhibited in PJH-treated mice. Conclusions This study demonstrates that PJH prevents respiratory inflammation and airway remodeling caused by CS with LPS exposure suggesting potential therapy for the treatment of COPD.Eun Bok BaekJin-hyung RhoEunhye JungChang-Seob SeoJin-Hee KimHyo-Jung KwunBMCarticleAirway remodelingChronic obstructive pulmonary diseasePalmijihwanghwanCigarette smokeInflammationOther systems of medicineRZ201-999ENBMC Complementary Medicine and Therapies, Vol 21, Iss 1, Pp 1-14 (2021)
institution DOAJ
collection DOAJ
language EN
topic Airway remodeling
Chronic obstructive pulmonary disease
Palmijihwanghwan
Cigarette smoke
Inflammation
Other systems of medicine
RZ201-999
spellingShingle Airway remodeling
Chronic obstructive pulmonary disease
Palmijihwanghwan
Cigarette smoke
Inflammation
Other systems of medicine
RZ201-999
Eun Bok Baek
Jin-hyung Rho
Eunhye Jung
Chang-Seob Seo
Jin-Hee Kim
Hyo-Jung Kwun
Protective effect of Palmijihwanghwan in a mouse model of cigarette smoke and lipopolysaccharide-induced chronic obstructive pulmonary disease
description Abstract Background Palmijihwanghwan (PJH) is a traditional medicine and eight constituents derived from PJH possess anti-inflammatory activities. However, the scientific evidence for its potential as a therapeutic agent for inflammatory lung disease has not yet been studied. In this study, we examined the protective effect of PJH in a mouse model of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke (CS) with lipopolysaccharide (LPS). Methods Mice received CS exposure for 8 weeks and intranasal instillation of LPS on weeks 1, 3, 5 and 7. PJH (100 and 200 mg/kg) was administrated daily 1 h before CS treatment for the last 4 weeks. Results Compared with CS plus LPS-exposed mice, mice in the PJH-treated group showed significantly decreased inflammatory cells count and reduced inflammatory cytokines including interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor alpha (TNF-α) levels in broncho-alveolar lavage fluid (BALF) and lung tissue. PJH also suppressed the phosphorylation of nuclear factor kappa B (NF-κB) and extracellular signal-regulated kinase1/2 (ERK1/2) caused by CS plus LPS exposure. Furthermore, CS plus LPS induced increases in matrix metallopeptidase (MMP)-7, MMP-9, and transforming growth factor-β (TGF-β) expression and collagen deposition that were inhibited in PJH-treated mice. Conclusions This study demonstrates that PJH prevents respiratory inflammation and airway remodeling caused by CS with LPS exposure suggesting potential therapy for the treatment of COPD.
format article
author Eun Bok Baek
Jin-hyung Rho
Eunhye Jung
Chang-Seob Seo
Jin-Hee Kim
Hyo-Jung Kwun
author_facet Eun Bok Baek
Jin-hyung Rho
Eunhye Jung
Chang-Seob Seo
Jin-Hee Kim
Hyo-Jung Kwun
author_sort Eun Bok Baek
title Protective effect of Palmijihwanghwan in a mouse model of cigarette smoke and lipopolysaccharide-induced chronic obstructive pulmonary disease
title_short Protective effect of Palmijihwanghwan in a mouse model of cigarette smoke and lipopolysaccharide-induced chronic obstructive pulmonary disease
title_full Protective effect of Palmijihwanghwan in a mouse model of cigarette smoke and lipopolysaccharide-induced chronic obstructive pulmonary disease
title_fullStr Protective effect of Palmijihwanghwan in a mouse model of cigarette smoke and lipopolysaccharide-induced chronic obstructive pulmonary disease
title_full_unstemmed Protective effect of Palmijihwanghwan in a mouse model of cigarette smoke and lipopolysaccharide-induced chronic obstructive pulmonary disease
title_sort protective effect of palmijihwanghwan in a mouse model of cigarette smoke and lipopolysaccharide-induced chronic obstructive pulmonary disease
publisher BMC
publishDate 2021
url https://doaj.org/article/a877c825ec9e4be9b8141268eeb05539
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