Analysis and modification of the metabolic antioxidative balance as risk factor for liver fibrosis in humanized, transgenic UGT1A SNP and wild type mice

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The hepatic fibrosis is a consequence of inflammation, infiltration of immunocompetent cells as well as effects of cytokines and chemokines, which are affected by oxidative stress and a stable metabolic antioxidative balance. UDP-glucuronosyltransferases are important effectors of this balance. Aim of the study is to investigate the regulatioin and interventional modification of these protective processes with respect to liver fibrosis during steatohepatitis, cholestasis and after ethanol exposure in a humanized transgenic UGT1A mouse model and to examine potential therapeutic approaches.