지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
이용수
초록· 키워드
오류제보하기
Objectives: Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation and irreversible airflow. This study aimed to evaluate the effects of GHX02 in a COPD-induced mouse model.
Methods: The COPD mouse model was established by exposure to cigarette smoke extract and lipopolysaccharide which were administered by intratracheal injection three times with a 7 day interval. GHX02 (100, 200, 400 mg/kg) and all other drugs were orally administrated for 14 days from Day 7 to Day 21.
Results: GHX02 significantly decreased the neutrophil counts in bronchoalveolar lavage fluid (BALF) and the number of CD4<SUP>+</SUP>, CD8<SUP>+</SUP>, CD69<SUP>+</SUP>, and CD11b<SUP>+</SUP>/GR1<SUP>+</SUP> cells in BALF and lung cells. GHX02 also suppressed the secretion of tumor necrosis factor-alpha (TNF-α), interleukin-17A, macrophage inflammatory protein 2 (MIP2), and chemokine (C–X–C motif) ligand 1 (CXCL-1) in BALF and ameliorated the lung pathological changes.
Conclusions: Thus, GHX02 effectively inhibited airway inflammation by inhibiting migration of inflammatory cells and expression of pro-inflammatory cytokines. Therefore, GHX02 may be a promising therapeutic agent for COPD.
Methods: The COPD mouse model was established by exposure to cigarette smoke extract and lipopolysaccharide which were administered by intratracheal injection three times with a 7 day interval. GHX02 (100, 200, 400 mg/kg) and all other drugs were orally administrated for 14 days from Day 7 to Day 21.
Results: GHX02 significantly decreased the neutrophil counts in bronchoalveolar lavage fluid (BALF) and the number of CD4<SUP>+</SUP>, CD8<SUP>+</SUP>, CD69<SUP>+</SUP>, and CD11b<SUP>+</SUP>/GR1<SUP>+</SUP> cells in BALF and lung cells. GHX02 also suppressed the secretion of tumor necrosis factor-alpha (TNF-α), interleukin-17A, macrophage inflammatory protein 2 (MIP2), and chemokine (C–X–C motif) ligand 1 (CXCL-1) in BALF and ameliorated the lung pathological changes.
Conclusions: Thus, GHX02 effectively inhibited airway inflammation by inhibiting migration of inflammatory cells and expression of pro-inflammatory cytokines. Therefore, GHX02 may be a promising therapeutic agent for COPD.
목차
Introduction
Materials and Methods
Results
Discussion
References
참고문헌 (34)
참고문헌 신청
[학술지(정기간행물)] - Woodruff PG / 2015 / Current concepts in targeting chronic obstructive pulmonary disease pharmacotherapy:making progress towards personalised management / The Lancet 385 (9979) : 1789 ~ 1798
[단행본] - Spurzem JR / 1994 / Pathogenesis of COPD. in Seminars in respiratory and critical care medicine 2005 / Thieme Medical Publishers
[학술지(정기간행물)] - Barnes PJ / 2016 / Inflammatory mechanisms in patients with chronic obstructive pulmonary disease / Journal of Allergy and Clinical Immunology 138 (1) : 16 ~ 27
[학술지(정기간행물)] - Cosio MG / 2009 / Immunologic aspects of chronic obstructive pulmonary disease / New England Journal of Medicine 360 (23) : 2445 ~ 2454
[학술지(정기간행물)] - Oostwoud L / 2016 / Apocynin and ebselen reduce influenza A virus-induced lung inflammation in cigarette smoke-exposed mice / Scientific reports 6 : 20983 ~
[단행본] - Spurzem JR / 1994 / Pathogenesis of COPD. in Seminars in respiratory and critical care medicine 2005 / Thieme Medical Publishers
[학술지(정기간행물)] - Barnes PJ / 2016 / Inflammatory mechanisms in patients with chronic obstructive pulmonary disease / Journal of Allergy and Clinical Immunology 138 (1) : 16 ~ 27
[학술지(정기간행물)] - Cosio MG / 2009 / Immunologic aspects of chronic obstructive pulmonary disease / New England Journal of Medicine 360 (23) : 2445 ~ 2454
[학술지(정기간행물)] - Oostwoud L / 2016 / Apocynin and ebselen reduce influenza A virus-induced lung inflammation in cigarette smoke-exposed mice / Scientific reports 6 : 20983 ~
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UCI(KEPA) : I410-ECN-0101-2019-519-000328679