Title : TAA-induced liver damage in KLF10 knockout mice
Abstract:
The liver plays an important role in regulating physiological functions such as detoxification of harmful substances. Liver injuries and diseases cause necrosis and apoptosis mainly due to an imbalance in cell protection pathway or detoxification. Therefore, liver injuries and diseases are serious health problems that threaten human health. Thioacetamide (TAA), an organosulfur compound is formerly used in leather processing laboratories, textile, and paper industries. Due to its effects on protein synthesis, RNA, DNA, and Gamma-glutamyl transpeptidase activity, is commonly used as a trigger agent to make animal disease model such as cirrhosis. Krüppel-like factors 10 is a transcription factor that has been in key cellular processes including cell proliferation, apoptosis, and differentiation. When the expression of KLF10 gene is deregulated, liver disease incidence is favored. In mouse liver, KLF10 regulates the expression of genes involved in glycolysis and gluconeogenesis. However, there is no evidence on the role of KLF10 in thioacetamide (TAA) mediated hepatotoxicity and its related damage. Upon this approach, we want to verify how this gene functions along the liver damage process as follows: Hepatic injury and its related enzyme activity, gene expression pattern, oxidative damage, inflammatory cytokines, and cellular processes including cell proliferation, apoptosis, and differentiation.
Audience take away:
• This can be helpful for researchers who are interested in liver disease area and related drug delivery.
• This study is about thioacetamide (TAA) mediated hepatotoxicity in KLF10 knockout mice.
• How KLF10 function during hepatic injury and its related enzymes activity, gene expression pattern, inflammatory cytokines and cellular processes including cell proliferation, apoptosis, and differentiation.
