الفهرس 
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Abstract
The present study was performed to investigate the possible effect of 17-AAG as an inhibitor for Hsp90 on controlling liver fibrosis induced experimentally. It aims at elucidating possible mechanisms underlying this potential effect. Treatment with 17-AAG concomitantly with TAA markedly along the second month attenuated TAA induced liver fibrosis. This was indicated by decreasing fibrosis score as revealed by examined liver sections histopathologically. The improvement was ensured by lowering elevated liver function biomarkers, reducing lipid peroxidation (low MDA levels) through restoring the antioxidant GSH hepatic capacity. Expressions of α-SMA, Col1A1 and TIMP-1 were lowered as well. These effects were more obvious with inhibitor higher dose (50 mg/kg). It was noticed that the 17-AAG 50 mg/kg increased NOx tissue level markedly. We postulate that the resulted NOx high level may have a beneficial role in the improvement in liver fibrosis degree. This role can be explained by the ability of NOx to counterbalance oxidative stress reducing HSCs proliferation and contractility. It could be concluded that treatment with Hsp90 inhibitor markedly controlled the development of experimentally induced liver fibrosis in mice received TAA. This role may be mainly attributed to its ability to decrease HSCs activation in addition to promoting their apoptosis.