ArticleCurrent pharmaceutical design2026
Exploring the Inhibitory Effects of Compounds for the Treatment of Liver Fibrosis: A Computational and Microscopic Approach.
Article in Current pharmaceutical design, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionHepatic fibrosis, a chronic liver injury caused by autoimmune, alcoholic, viral, and non-alcoholic fatty liver disorders, leads to cirrhosis. Proteins that stimulate HSCs to initiate wound healing are suppressed as part of the treatment. This study aims to identify potential inhibitors of COX2, integrin, PDGF, TGF-β, and protein kinase C, validate in silico results, and compare inhibitory effects using scanning electron microscopy.
methodsA database was used to identify proteins of interest, and inhibitors against specific proteins previously reported were selected. Ligand-protein interactions were evaluated through docking simulations using MOE, and the resulting complexes were analyzed using SwissADME. The study involved five groups of male rats, each weighing 200-240 g. The first group was a control without treatment or fibrosis induction, the second group was a negative control with CCl4 injection, and groups 3, 4, and 5 received silymarin, rutin, and sorafenib treatments, respectively, in addition to CCl4.
resultsThe study demonstrated that three compounds-silymarin, rutin, and sorafenib-can inhibit six different proteins. Rutin interacts with multiple proteins and has a docking score of -7.5220. It acts as a P-gp substrate, crosses the blood-brain barrier persistently, and shows high gastrointestinal absorption. DISCUSSION: This work demonstrates how computer-aided drug design can be used to identify potent molecules targeting COX2, PKC, integrin, Claudin 2, TGF-β, and PDGF, advancing drug management and therapy of liver fibrosis. In vivo studies indicate that silymarin is the most effective compound for reducing enzyme levels.
conclusionMicroscopic examination of the CCl4 group indicated hepatocellular necrosis, inflammation, fibrosis, and bile duct proliferation, characterized by enlarged ductal cells, bile ductules, and extensive hepatocyte necrosis. Treatment with rutin, silymarin, and sorafenib improved CCl4-induced liver damage. Among these, rutin treatment restored liver architecture, reduced inflammation, lessened fibrosis, and caused minimal hepatocellular damage. Silymarin treatment reduced fibrosis, tissue damage, and inflammatory cell infiltration. Sorafenib treatment caused minimal to moderate hepatocyte damage while improving liver function by decreasing inflammation and fibrosis.
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