دورية أكاديمية
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Mefunidone ameliorates lipopolysaccharide-induced acute lung injury through inhibiting MAPK signaling pathway and enhancing Nrf2 pathway.

التفاصيل البيبلوغرافية
العنوان: Mefunidone ameliorates lipopolysaccharide-induced acute lung injury through inhibiting MAPK signaling pathway and enhancing Nrf2 pathway.
المؤلفون: Yao TT; Department of Pulmonary and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China., Zhang Y; Department of Pulmonary and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China., He RL; Department of Pulmonary and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China., Lv X; Department of Nephrology, Xiangya Hospital, Central South University, Changsha, China., He YJ; Department of Pulmonary and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China., Li MY; Department of Pulmonary and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China., Han YY; Department of Nephrology, Xiangya Hospital, Central South University, Changsha, China., Long LZ; Department of Pulmonary and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China., Jiang GL; Department of Pulmonary and Critical Care Medicine, Xiangya Hospital, Central South University, Changsha, China., Cheng XY; Department of Pulmonary and Critical Care Medicine, Xiangya Hospital, Central South University, Changsha, China., Hu GY; Department of Medicinal Chemistry, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha, China; Hunan Key Laboratory of Organ Fibrosis, Changsha, China., Li QB; Department of Medicinal Chemistry, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha, China; Hunan Key Laboratory of Organ Fibrosis, Changsha, China., Tao LJ; Department of Nephrology, Xiangya Hospital, Central South University, Changsha, China; Hunan Key Laboratory of Organ Fibrosis, Changsha, China; National International Collaborative Research Center for Medical Metabolomics, Changsha, China., Meng J; Department of Pulmonary and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China; Hunan Key Laboratory of Organ Fibrosis, Changsha, China; National International Collaborative Research Center for Medical Metabolomics, Changsha, China. Electronic address: mengjie@csu.edu.cn.
المصدر: International immunopharmacology [Int Immunopharmacol] 2022 Dec; Vol. 113 (Pt A), pp. 109263. Date of Electronic Publication: 2022 Nov 02.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier Science Country of Publication: Netherlands NLM ID: 100965259 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1878-1705 (Electronic) Linking ISSN: 15675769 NLM ISO Abbreviation: Int Immunopharmacol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Amsterdam ; New York : Elsevier Science, c2001-
مواضيع طبية MeSH: Pyridones*/pharmacology , Piperazines*/pharmacology, Animals ; Mice ; Inflammation/metabolism ; Lipopolysaccharides ; Lung/pathology ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinases/metabolism ; NF-E2-Related Factor 2/metabolism ; Signal Transduction
مستخلص: Background and Objective: Acute lung injury (ALI) is a life-threatening disease which has high mortality and lacks effective pharmacological treatments. Excessive inflammation and oxidative stress are the key pathogenesis of ALI. Mefunidone (MFD), a novel small molecule compound, displayed anti-inflammation and anti-oxidative stress effects on streptozocin (STZ) and db/db mice in our previous studies. In this study, we aimed to investigate the effects of MFD on lipopolysaccharide (LPS)-induced ALI and explore the potential molecular mechanisms.
Methods: We investigated the effects of MFD on LPS-induced ALI mouse model and LPS-stimulated immortalized mouse bone marrow-derived macrophages (iBMDMs).
Results: MFD could alleviate pulmonary structure disorder and attenuate pulmonary neutrophils infiltration induced by LPS. MFD could also decreased proinflammatory cytokines release and reduce reactive oxygen species (ROS) generation stimulated by LPS. Further, MFD could significantly reduce LPS-induced phosphorylation levels of mitogen-activated protein kinase (MAPK), increase expression of nuclear factor-erythroid 2 related factor 2 (Nrf2) and restore the expressions of antioxidant enzymes.
Conclusion: Our results firstly supported that MFD effectively protected LPS-induced ALI against inflammation and oxidative stress through inhibiting MAPK signaling pathway and activating Nrf2 pathway.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)
فهرسة مساهمة: Keywords: Acute lung injury; Inflammation; MAPK; Mefunidone; Nrf2; Oxidative stress
المشرفين على المادة: 0 (1-(4-((3-(4-methylpiperazin-1-yl)propyl)amino)benzyl)-5-(trifluoromethyl)pyridin-2(1H)-one)
0 (Lipopolysaccharides)
EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
0 (NF-E2-Related Factor 2)
0 (Pyridones)
0 (Piperazines)
تواريخ الأحداث: Date Created: 20221105 Date Completed: 20221213 Latest Revision: 20221213
رمز التحديث: 20221214
DOI: 10.1016/j.intimp.2022.109263
PMID: 36334370
قاعدة البيانات: MEDLINE
الوصف
تدمد:1878-1705
DOI:10.1016/j.intimp.2022.109263