Effect of curcumin and gliotoxin on rat liver myofibroblasts culture

Since 1990s, when it was demonstrated by Hammel and others, that liver fibrosis is reversible, researchers and physicians actively search for new antifibrotic therapies. In recent years knowledge of liver fibrosis pathophysiology has greatly advanced and new cellular and molecular mechanisms were described. The cells that determine extracellular matrix components distribution are myofibroblasts, but their origin is diverse. They can be activated hepatic stellate cells (HSC), portal fibroblasts (PF) or circulating mesenchymal stem cells of bone marrow. Activation of HSC and PF and their fibrogenic potential is upregulated by transcription factor NF-B. Among large number of substrates to inhibit NF-B and induce apoptosis we chose curcumin and gliotoxin. Primarily in current work we optimized the explantation culture method for isolation of hepatic myofibroblasts and received two different cultures - myofibroblasts of HSC and PF origin. Exposition of 50 ?M curcumin and 0,1 ?M gliotoxi

Effect of curcumin and gliotoxin on rat liver myofibroblasts culture

Since 1990s, when it was demonstrated by Hammel and others, that liver fibrosis is reversible, researchers and physicians actively search for new antifibrotic therapies. In recent years knowledge of liver fibrosis pathophysiology has greatly advanced and new cellular and molecular mechanisms were described. The cells that determine extracellular matrix components distribution are myofibroblasts, but their origin is diverse. They can be activated hepatic stellate cells (HSC), portal fibroblasts (PF) or circulating mesenchymal stem cells of bone marrow. Activation of HSC and PF and their fibrogenic potential is upregulated by transcription factor NF-B. Among large number of substrates to inhibit NF-B and induce apoptosis we chose curcumin and gliotoxin. Primarily in current work we optimized the explantation culture method for isolation of hepatic myofibroblasts and received two different cultures - myofibroblasts of HSC and PF origin. Exposition of 50 ?M curcumin and 0,1 ?M gliotoxi