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10.4196/kjpp.2016.20.3.305

http://scihub22266oqcxt.onion/10.4196/kjpp.2016.20.3.305
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suck abstract from ncbi


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pmid27162485
      Korean+J+Physiol+Pharmacol 2016 ; 20 (3 ): 305-14
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  • NecroX-5 exerts anti-inflammatory and anti-fibrotic effects via modulation of the TNF?/Dcn/TGF?1/Smad2 pathway in hypoxia/reoxygenation-treated rat hearts #MMPMID27162485
  • Thu VT ; Kim HK ; Long le T ; Thuy TT ; Huy NQ ; Kim SH ; Kim N ; Ko KS ; Rhee BD ; Han J
  • Korean J Physiol Pharmacol 2016[May]; 20 (3 ): 305-14 PMID27162485 show ga
  • Inflammatory and fibrotic responses are accelerated during the reperfusion period, and excessive fibrosis and inflammation contribute to cardiac malfunction. NecroX compounds have been shown to protect the liver and heart from ischemia-reperfusion injury. The aim of this study was to further define the role and mechanism of action of NecroX-5 in regulating infl ammation and fi brosis responses in a model of hypoxia/reoxygenation (HR). We utilized HR-treated rat hearts and lipopolysaccharide (LPS)-treated H9C2 culture cells in the presence or absence of NecroX-5 (10 µmol/L) treatment as experimental models. Addition of NecroX-5 signifi cantly increased decorin (Dcn) expression levels in HR-treated hearts. In contrast, expression of transforming growth factor beta 1 (TGF?1) and Smad2 phosphorylation (pSmad2) was strongly attenuated in NecroX-5-treated hearts. In addition, signifi cantly increased production of tumor necrosis factor alpha (TNF?), TGF?1, and pSmad2, and markedly decreased Dcn expression levels, were observed in LPS-stimulated H9C2 cells. Interestingly, NecroX-5 supplementation effectively attenuated the increased expression levels of TNF?, TGF?1, and pSmad2, as well as the decreased expression of Dcn. Thus, our data demonstrate potential antiinflammatory and anti-fibrotic effects of NecroX-5 against cardiac HR injuries via modulation of the TNF?/Dcn/TGF?1/Smad2 pathway.
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