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

人源化转基因 UGT1A SNP 和野生型小鼠中代谢抗氧化平衡作为肝纤维化危险因素的分析和修改

• 批准号: 268209133
• 负责人: Professor Dr. Christian Strassburg
• 金额: --
• 依托单位: Medizinische Klinik und Poliklinik I - Allgemeine Innere Medizin
• 依托单位国家: 德国
• 项目类别: Research Grants
• 财政年份: 2015
• 资助国家: 德国
• 起止时间: 2014-12-31 至 2017-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/268209133?language=en
• 关键词: Analysis; modification; metabolic; antioxidative; balance

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.

肝纤维化是炎症、免疫活性细胞浸润以及细胞因子和趋化因子作用的结果，细胞因子和趋化因子受氧化应激和稳定的代谢抗氧化平衡的影响。UDP-葡萄糖醛酸基转移酶是这种平衡的重要影响因素。本研究的目的是在人源化的转基因UGT1A小鼠模型中，研究这些保护过程在脂肪性肝炎、胆汁淤积和酒精暴露后肝纤维化中的调节和干预性修改，并探索潜在的治疗方法。