Document Detail


Oxymatrine protects against myocardial injury via inhibition of JAK2/STAT3 signaling in rat septic shock.
MedLine Citation:
PMID:  23404057     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Oxymatrine (OMT), an alkaloid extracted from Sophora japonica (kushen), is used to treat inflammatory diseases and various types of cancer in traditional Chinese medicine. However, the cellular and molecular mechanisms underlying the anti‑inflammatory activity of OMT remain poorly understood. The present study explored the protective effect of OMT on myocardial injury in rats with septic shock by inhibiting the activation of the janus kinase‑signal transducer and activator of transcription (JAK/STAT) signaling pathway. OMT treatment was found to significantly inhibit the activation of JAK2 and STAT3 in myocardial tissue. It also attenuated the expression of pro‑inflammatory cytokines, including interleukin‑1β and tumor necrosis factor‑α. In addition, OMT exhibited anti‑inflammatory properties as heart function and myocardial contractility was improved and pathological and ultrastructural injury was prevented in myocardial tissue induced by septic shock. The results indicate that OMT exhibits substantial therapeutic potential for the treatment of septic shock‑induced myocardial injury through inhibition of the JAK2/STAT3 signaling pathway.
Authors:
Minghao Zhang; Xiuyu Wang; Xiumei Wang; Xiaolin Hou; Peng Teng; Yideng Jiang; Linna Zhang; Xiaoling Yang; Jue Tian; Guizhong Li; Jun Cao; Hua Xu; Yunhong Li; Yin Wang
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2013-2-08
Journal Detail:
Title:  Molecular medicine reports     Volume:  -     ISSN:  1791-3004     ISO Abbreviation:  Mol Med Report     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-2-13     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101475259     Medline TA:  Mol Med Report     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Department of Pathophysiology and Neurobiology, Basic Medical College, Center of Scientific Technology, Ningxia Medical University, Yinchuan 750004, P.R. China.
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