|کد مقاله||کد نشریه||سال انتشار||مقاله انگلیسی||ترجمه فارسی||نسخه تمام متن|
|5529312||1401692||2017||8 صفحه PDF||سفارش دهید||دانلود رایگان|
BackgroundHepatic fibrosis is characterized by a progressive accumulation of fibrillar extracellular matrix (ECM) proteins, produced by activated myofibroblasts which are modulated by both profibrotic and antifibrotic factors.ObjectiveTo evaluate in vivo the expression of pro-fibrotic molecules like avÎ²6 integrin, transforming growth factor-Î² (TGF-Î²), Smad3, connective tissue growth factor (CTGF) and mammalian target of Rapamycin (mTOR), as well as anti-fibrotic peroxisome proliferator-activated receptor-Î³ (PPARÎ³) in an experimental model of chronic hepatitis-associated fibrosis induced by intraperitoneal administration of dimethylnitrosamine (DMN) in mice.MethodsChronic hepatitis was induced in 12 Smad3 wild-type (WT) and 12 knock-out (KO) mice by intraperitoneal DMN administration. Histological, morphometric and immunohistochemical analyses using Î±-smooth muscle actin (Î±-SMA), collagen types I-III, TGF-Î²1, Smad3, avÎ²6 integrin, CTGF, mTOR and PPARÎ³ antibodies were performed.ResultsThe liver of DMN-treated Smad3 WT mice showed a higher degree of hepatic accumulation of connective tissue compared to KO mice. The expression of Î±-SMA, collagen I-III and CTGF was increased in Smad3 WT compared to KO mice treated with DMN, associated with a concomitant up-regulation of avÎ²6, TGFÎ², Smad3, and mTOR and a reduction in PPARÎ³ expression.ConclusionsThese results suggest a possible interaction between pro-fibrotic and anti-fibrotic molecules in the development of hepatic fibrosis.
Journal: Pathology - Research and Practice - Volume 213, Issue 1, January 2017, Pages 58-65