The Mechanism Of Nuclear Factor -κBin Immune Liver Injury

Immune liver injury can be induced by cytokines and cells stimulated by various cytokines produced abnormally activated T-lymphocytes. Immune liver injury plays a pivotal role in many liver diseases. NF-KB is a transcription factor regulating the expression of numerous cytokine genes, and it is found in almost all cells. It is found to be involved in many pathological processes such as immunity, inflammation and oxidative stress. It was presumed that NF-KB might participate in immune liver injury.Male B ALB/c mice were treated with con A to establish the immune Hver injury model that had been proved to be mainly caused by the abnormally activated T cells. In this model, ALT increased significantly. Necrosis and apoptosis was observed and NF- K B was activated The increase of TNF s NO was followed by the activation of NF- K B. ET also increased In another group PDTC was admitted 30 min before con A injection. Necrosis and apoptosis decreased Activity of NF- K B was lower than that in the model without PDTC, and the concentration of TNF N NO and ET was also lower than that in the first model. NF- K B regulated the expression of proinflarnrnatory genes. NF- K B increased in the immune liver injury model and inhabitation ofNF- K B resulted in the decreased liver injury. It is inferred that NF- K B maybe participate in the cytokme-mediated liver injury. That ET increased after NF- K B was activated indicated some relationship between NF- K B and ET.