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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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) |
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Airway remodeling Chronic obstructive pulmonary disease Palmijihwanghwan Cigarette smoke Inflammation Other systems of medicine RZ201-999 |
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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 |
work_keys_str_mv |
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