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Inhibitory Effect Of Icariin On Cardiac Fibrosis Rat Induced By Abdominal Aortic Coarctation

Posted on:2015-03-29Degree:MasterType:Thesis
Country:ChinaCandidate:L M ZhangFull Text:PDF
GTID:2254330422474746Subject:Pharmacology
Abstract/Summary:PDF Full Text Request
Objective: To observe inhibitory effect of Icariin on cardiac fibrosis rat induced byabdominal aortic coarctation and explore the mechanisms.Methods: The abdominal aortic coarctation of rats model was produced. Animals werethen treated (i.g) with distilled water (sham operation group and model group) or Ica (40mg/kg/d、80mg/kg/d) by (i.g). After50days of Icariin treated, the Myocardial morphologyin rats induced by abdominal aortic coarctation was detected by HE and MASSON,the degreeof I,III collegn proliferation in SD rat heart were evaluated by Image-Pro Plus,and thepNF-κB(p65) positive protein expression is calculated by Image-Pro Plus too.The proteinexpressions of phosphorylation TGF-β1, p-Smad2, MMP-9, TIMP-1, PPARα,pNF-κB(p65),IκBα,TNF-α were examined by Western-blot and then analyzed withImage-Pro Plus. The mRNA expression of TGF-β1,Smad2,MMP-9,TIMP-1,PPARαPPARγ,NF-κB,TNF-α levels were detected by Real-Time RT-PCR.Results: Compared with Sham group, myocardial fibrosis rats colored dull,sluggished, food intaken decreased, and lossed weight. We also saw myocardial hypertrophy, degeneration, necrosis, disorder arrangent, inflammatory cell infiltration,and the increased perspective of fibrosis unit area(P <0.01) in myocardial fibrosisgroup.The I,III collagen significantly were increased induced,at the same time, the expressions of protein and mRNA of TGF-β1, p-Smad2,MMP-9, TIMP-1, PPARγ, pNF-κB(p65), IκBα, TNF-α were increased significantly and the PPARαexpression were decreased in abdominal aortic coarctation groups.Compared abdominal aortic coarctation model group, the I,III collagen significantly were decreased by Ica; the expressions of protein and mRNA of TGF-β1, p-Smad2,MMP-9,TI MP-1, PPARγ, pNF-κB(p65), IκBα, TNF-α were decreased significantly and thePPARα expression were increased in Ica mediation groups.Conclusions: Ica can significantly attenuate the CFs induced by pressure overloadedin rats; The anti-fibrosis effect of Ica appears to be due, at least in part, todecrease TGF-β1,p-Smad2,MMP-9,TIMP-1proteins and to increase PPARα protein.
Keywords/Search Tags:Ica, TNF-α, PPARγ, PPARα, TGF-β1, p-Smad2, MMP-9, TIMP-1, abdominal aortic coarctation, myocardial fibrosis
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