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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| Format: | Article |
| Language: | English |
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Elsevier
2023-11-01
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| Series: | Heliyon |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2405844023081227 |
| _version_ | 1797429994295656448 |
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| author | Yang Miao Yue Yang Xiaohe Li Lingxin Meng Jiahe Mao Jianwei Zhang Jingjing Gao Cheng Yang Xiaoting Gu Honggang Zhou Yanping Zhang |
| author_facet | Yang Miao Yue Yang Xiaohe Li Lingxin Meng Jiahe Mao Jianwei Zhang Jingjing Gao Cheng Yang Xiaoting Gu Honggang Zhou Yanping Zhang |
| author_sort | Yang Miao |
| collection | DOAJ |
| 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. |
| first_indexed | 2024-03-09T09:21:18Z |
| format | Article |
| id | doaj.art-9080f6b7336144d8b451a0406ed39bd0 |
| institution | Directory Open Access Journal |
| issn | 2405-8440 |
| language | English |
| last_indexed | 2024-03-09T09:21:18Z |
| publishDate | 2023-11-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Heliyon |
| spelling | doaj.art-9080f6b7336144d8b451a0406ed39bd02023-12-02T07:00:57ZengElsevierHeliyon2405-84402023-11-01911e20914Imrecoxib attenuates bleomycin-induced pulmonary fibrosis in miceYang Miao0Yue Yang1Xiaohe Li2Lingxin Meng3Jiahe Mao4Jianwei Zhang5Jingjing Gao6Cheng Yang7Xiaoting Gu8Honggang Zhou9Yanping Zhang10State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Haihe Education Park, 38 Tongyan Road, Tianjin, 300353, ChinaState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Haihe Education Park, 38 Tongyan Road, Tianjin, 300353, ChinaState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Haihe Education Park, 38 Tongyan Road, Tianjin, 300353, ChinaState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Haihe Education Park, 38 Tongyan Road, Tianjin, 300353, ChinaState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Haihe Education Park, 38 Tongyan Road, Tianjin, 300353, ChinaState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Haihe Education Park, 38 Tongyan Road, Tianjin, 300353, ChinaTianjin Jikun Technology Co., Ltd. Tianjin, 301700, ChinaState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Haihe Education Park, 38 Tongyan Road, Tianjin, 300353, ChinaState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Haihe Education Park, 38 Tongyan Road, Tianjin, 300353, China; Corresponding author.State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Haihe Education Park, 38 Tongyan Road, Tianjin, 300353, China; Corresponding author.The Second Department of Respiratory and Critical Care Medicine, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, China; Corresponding author.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.http://www.sciencedirect.com/science/article/pii/S2405844023081227Idiopathic pulmonary fibrosisImrecoxibInflammationTGF-β1ERK1/2 |
| spellingShingle | Yang Miao Yue Yang Xiaohe Li Lingxin Meng Jiahe Mao Jianwei Zhang Jingjing Gao Cheng Yang Xiaoting Gu Honggang Zhou Yanping Zhang Imrecoxib attenuates bleomycin-induced pulmonary fibrosis in mice Heliyon Idiopathic pulmonary fibrosis Imrecoxib Inflammation TGF-β1 ERK1/2 |
| 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 | Idiopathic pulmonary fibrosis Imrecoxib Inflammation TGF-β1 ERK1/2 |
| url | http://www.sciencedirect.com/science/article/pii/S2405844023081227 |
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