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Imrecoxib attenuates bleomycin-induced pulmonary fibrosis in mice

Idiopathic pulmonary fibrosis (IPF) is an incurable chronic progressive disease with a low survival rate and ineffective therapeutic options. We examined the effects of imrecoxib, a nonsteroidal anti-inflammatory drug, on experimental pulmonary fibrosis. The mouse IPF model was established by intrat...

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Autores principales: Miao, Yang, Yang, Yue, Li, Xiaohe, Meng, Lingxin, Mao, Jiahe, Zhang, Jianwei, Gao, Jingjing, Yang, Cheng, Gu, Xiaoting, Zhou, Honggang, Zhang, Yanping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10663740/
https://www.ncbi.nlm.nih.gov/pubmed/38027732
http://dx.doi.org/10.1016/j.heliyon.2023.e20914
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author Miao, Yang
Yang, Yue
Li, Xiaohe
Meng, Lingxin
Mao, Jiahe
Zhang, Jianwei
Gao, Jingjing
Yang, Cheng
Gu, Xiaoting
Zhou, Honggang
Zhang, Yanping
author_facet Miao, Yang
Yang, Yue
Li, Xiaohe
Meng, Lingxin
Mao, Jiahe
Zhang, Jianwei
Gao, Jingjing
Yang, Cheng
Gu, Xiaoting
Zhou, Honggang
Zhang, Yanping
author_sort Miao, Yang
collection PubMed
description Idiopathic pulmonary fibrosis (IPF) is an incurable chronic progressive disease with a low survival rate and ineffective therapeutic options. We examined the effects of imrecoxib, a nonsteroidal anti-inflammatory drug, on experimental pulmonary fibrosis. The mouse IPF model was established by intratracheal instillation of bleomycin. From Day 0 to Day 13, the mice were orally administered imrecoxib (100 mg/kg) and pirfenidone (200 mg/kg) daily, and from Day 7 to Day 13, the mice were orally administered pirfenidone and imrecoxib daily. The tissues were dissected on the 14th day. Mouse body weight was measured, and histopathological examination and hydroxyproline content analysis confirmed that the administration of imrecoxib exerted a similar effect to pirfenidone. Compared with bleomycin-induced mice, imrecoxib-treated mice showed significantly reduced inflammatory factor expression (IL-1 and TNF-α) and inflammatory cell numbers (macrophages, lymphocytes, and neutrophils) in BALF (bronchoalveolar lavage fluid). Our experiment tested the ability of imrecoxib to inhibit the signal pathway involved in gene expression induced by TGF-β1 in the NIH-3T3 cell line in vitro. Western blotting showed that imrecoxib (20 μM and 40 μM) inhibited the expression of fibronectin, type I collagen and CTGF. In addition, imrecoxib reduced the levels of p-ERK1/2. The changes in the expression of related proteins in mouse lung tissue were similar to those in cells. In summary, our findings suggested that the administration of imrecoxib prevented and treated murine IPF by inhibiting inflammation and the TGF-β1-ERK1/2 signaling pathway.
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spelling pubmed-106637402023-11-03 Imrecoxib attenuates bleomycin-induced pulmonary fibrosis in mice Miao, Yang Yang, Yue Li, Xiaohe Meng, Lingxin Mao, Jiahe Zhang, Jianwei Gao, Jingjing Yang, Cheng Gu, Xiaoting Zhou, Honggang Zhang, Yanping Heliyon Research Article Idiopathic pulmonary fibrosis (IPF) is an incurable chronic progressive disease with a low survival rate and ineffective therapeutic options. We examined the effects of imrecoxib, a nonsteroidal anti-inflammatory drug, on experimental pulmonary fibrosis. The mouse IPF model was established by intratracheal instillation of bleomycin. From Day 0 to Day 13, the mice were orally administered imrecoxib (100 mg/kg) and pirfenidone (200 mg/kg) daily, and from Day 7 to Day 13, the mice were orally administered pirfenidone and imrecoxib daily. The tissues were dissected on the 14th day. Mouse body weight was measured, and histopathological examination and hydroxyproline content analysis confirmed that the administration of imrecoxib exerted a similar effect to pirfenidone. Compared with bleomycin-induced mice, imrecoxib-treated mice showed significantly reduced inflammatory factor expression (IL-1 and TNF-α) and inflammatory cell numbers (macrophages, lymphocytes, and neutrophils) in BALF (bronchoalveolar lavage fluid). Our experiment tested the ability of imrecoxib to inhibit the signal pathway involved in gene expression induced by TGF-β1 in the NIH-3T3 cell line in vitro. Western blotting showed that imrecoxib (20 μM and 40 μM) inhibited the expression of fibronectin, type I collagen and CTGF. In addition, imrecoxib reduced the levels of p-ERK1/2. The changes in the expression of related proteins in mouse lung tissue were similar to those in cells. In summary, our findings suggested that the administration of imrecoxib prevented and treated murine IPF by inhibiting inflammation and the TGF-β1-ERK1/2 signaling pathway. Elsevier 2023-11-03 /pmc/articles/PMC10663740/ /pubmed/38027732 http://dx.doi.org/10.1016/j.heliyon.2023.e20914 Text en © 2023 The Authors https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Research Article
Miao, Yang
Yang, Yue
Li, Xiaohe
Meng, Lingxin
Mao, Jiahe
Zhang, Jianwei
Gao, Jingjing
Yang, Cheng
Gu, Xiaoting
Zhou, Honggang
Zhang, Yanping
Imrecoxib attenuates bleomycin-induced pulmonary fibrosis in mice
title Imrecoxib attenuates bleomycin-induced pulmonary fibrosis in mice
title_full Imrecoxib attenuates bleomycin-induced pulmonary fibrosis in mice
title_fullStr Imrecoxib attenuates bleomycin-induced pulmonary fibrosis in mice
title_full_unstemmed Imrecoxib attenuates bleomycin-induced pulmonary fibrosis in mice
title_short Imrecoxib attenuates bleomycin-induced pulmonary fibrosis in mice
title_sort imrecoxib attenuates bleomycin-induced pulmonary fibrosis in mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10663740/
https://www.ncbi.nlm.nih.gov/pubmed/38027732
http://dx.doi.org/10.1016/j.heliyon.2023.e20914
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