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Effect of scutellarin on JAK/STAT pathway in myocardial ischemia reperfusion rats (LB561)
Author(s) -
Yang Weimin,
Li Lin,
Cai Donghua,
Li Jiaxun,
Du Yue,
Guo Tao
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb561
Subject(s) - scutellarin , western blot , stat3 , stat protein , janus kinase , immunohistochemistry , jak stat signaling pathway , stat , janus kinase 2 , medicine , phosphorylation , ischemia , myocardial ischemia , pharmacology , reperfusion injury , chemistry , biochemistry , receptor , tyrosine kinase , gene
Animal studies have demonstrated that scutellarin (SCU) limits damage after myocardial ischemia injury. However, the underlying molecular mechanisms of SCU protecting against myocardial injury induced by ischemia reperfusion (IR) are not well known. This study examined whether SCU protects against myocardial IR injury in rats is mediated by the Janus kinase and signal transducer and activator of transcription (JAK/STAT) pathway. Protein expression of JAK2/STAT3 and phosphorylative products were assessed by Western blot and immunohistochemistry methods in myocardial tissue from myocardial IR rats pretreated with SCU (45 and 90 mg/kg, iv). Western blot and immunohistochemistry assays showed that myocardial IR injury caused significant increases of phosphorylated JAK2 (p‐JAK2) and phosphorylated STAT3 (p‐STATS) levels in the rat myocardial IR model. SCU (45 and 90 mg/kg, iv) significantly reduced ischemic size, and decreased histological p‐JAK2 and p‐STATS expression. SCU attenuates myocardial IR injury which involved in JAK/STAT signaling pathway. Grant Funding Source : Supported by grants from the National Natural Science Foundation of China (Nos. 30960450 and 81173110) and Yunnan Provincial Science and Technology Department (Nos. 2011FA022, 2012BC012, 2008CD054, and 2008ZC111M).