Characterization of Quin-C1 for its anti-inflammatory property in a mouse model of bleomycin-induced lung injury
文献类型:期刊论文
作者 | He, Min1; Cheng, Ni2; Gao, Wei-wei1; Zhang, Meng1; Zhang, Yue-yun1; Ye, Richard D.2; Wang, Ming-wei1![]() |
刊名 | ACTA PHARMACOLOGICA SINICA
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出版日期 | 2011-05 |
卷号 | 32期号:5页码:601-610 |
关键词 | Quin-C1 anti-inflammation bleomycin lung injury formyl peptide receptor cytokines |
ISSN号 | 1671-4083 |
DOI | 10.1038/aps.2011.4 |
文献子类 | Article |
英文摘要 | Aim: To study the in vivo effects of Quin-C1, a highly specific agonist for formyl peptide receptor 2 (FPR2/ALX), in a mouse model of bleomycin (BLM)-induced lung injury. Methods: Male ICR mice were injected intratracheally with BLM (d 0), and intraperitoneally with Quin-C1 (0.2 mg/d) or vehicle between d 1 and d 28, during which pulmonary inflammation was monitored. A similar regimen was carried out between d 5 and d 28 to differentiate anti-inflammatory from anti-fibrotic effects. During the treatment, leukocyte numbers in bronchoalveolar lavage fluid (BALF) were counted, and FPR2/ALX transcripts, tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), the mouse keratinocyte-derived chemokine (KC), transforming growth factor beta 1 (TGF-beta 1) and C-X-C motif chemokine 10 (CXCL10) expression levels in the lung tissue were also measured. Both hydroxyproline content and histological changes were examined on d 28 to assess the severity of lung fibrosis. Results: BLM caused a significant increase in expression levels of all the selected cytokines and chemokines, as well as a thickening of the alveolar wall. Treatment with Quin-C1 significantly reduced the neutrophil and lymphocyte counts in BALF, diminished expression of TNF-alpha, IL-1 beta, KC, and TGF-beta 1, and decreased collagen deposition in lung tissue. The treatment also lowered the content of lung hydroxyproline. Quin-C1 did not ameliorate lung fibrosis when the treatment was started 5 d after the BLM challenge, suggesting that the protection may be attributed to its anti-inflammatory effects. Exposure to BLM or BLM plus Quin-C1 did not change the level of FPR2/ALX transcripts (mFpr1, mFpr2, and Lxa4r) in the lung tissue. Conclusion: The results demonstrate an anti-inflammatory role for Quin-C1 in bleomycin-induced lung injury, which may be further explored for therapeutic applications. |
WOS关键词 | INDUCED PULMONARY-FIBROSIS ; FORMYL-PEPTIDE RECEPTOR ; ASPIRIN-TRIGGERED LIPOXIN ; PROTEIN-COUPLED RECEPTORS ; LISTERIA-MONOCYTOGENES ; LIPID MEDIATORS ; TGF-BETA ; KAPPA-B ; MICE ; LIGAND |
资助项目 | Ministry of Science and Technology of China[2009ZX09302-001] ; Shanghai Municipality government[08430703200] ; Shanghai Municipality government[09DZ2291200] ; National Institutes of Health, USA[AI033503] |
WOS研究方向 | Chemistry ; Pharmacology & Pharmacy |
语种 | 英语 |
CSCD记录号 | CSCD:4190576 |
WOS记录号 | WOS:000290276300008 |
出版者 | ACTA PHARMACOLOGICA SINICA |
源URL | [http://119.78.100.183/handle/2S10ELR8/278544] ![]() |
专题 | 国家新药筛选中心 中科院受体结构与功能重点实验室 新药研究国家重点实验室 |
通讯作者 | Wang, Ming-wei |
作者单位 | 1.Chinese Acad Sci, Shanghai Inst Mat Med, Natl Ctr Drug Screening, State Key Lab Drug Res, Shanghai 201203, Peoples R China; 2.Univ Illinois, Dept Pharmacol, Coll Med, Chicago, IL 60612 USA |
推荐引用方式 GB/T 7714 | He, Min,Cheng, Ni,Gao, Wei-wei,et al. Characterization of Quin-C1 for its anti-inflammatory property in a mouse model of bleomycin-induced lung injury[J]. ACTA PHARMACOLOGICA SINICA,2011,32(5):601-610. |
APA | He, Min.,Cheng, Ni.,Gao, Wei-wei.,Zhang, Meng.,Zhang, Yue-yun.,...&Wang, Ming-wei.(2011).Characterization of Quin-C1 for its anti-inflammatory property in a mouse model of bleomycin-induced lung injury.ACTA PHARMACOLOGICA SINICA,32(5),601-610. |
MLA | He, Min,et al."Characterization of Quin-C1 for its anti-inflammatory property in a mouse model of bleomycin-induced lung injury".ACTA PHARMACOLOGICA SINICA 32.5(2011):601-610. |
入库方式: OAI收割
来源:上海药物研究所
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