Research On Emodin Regulated Astrocytes Functional By Interfer α-7-nAChRs And The Relation With Hepatic Encephalopathy

Hepatic encephalopathy (HE) is a disease drived from severity liver damage, symptom include spirit and activity disorder, and is the most commn reason for the death of final liver disease. Currently, HE devided into three types A B and C. Three types HE is respectively related with acute liver failure, hide liver disease and chronic liver disease. At present, the mechanism of HE is unclear, and have no effective means of prevention. HE is seriously affect quality of life and survival of patients. So research on the HE is very important for the health.Aim:In overall, cellular and molecular level, to clarify a7-nAChRs in the pathogenesis of hepatic encephalopathy and its mechanism of regulation, anti-inflammatory pathway regulated emodin observed for choline, for exploring targeting specific nicotinic receptor regulation agents, prevention and treatment of hepatic encephalopathy provide academic basis. Proposed and verified "emodin neuroprotective role in hepatic encephalopathy" hypothesis. Clarify a7-nAChRs on the regulation of astrocyte function and its mechanism, to further expand the field of biology research nicotinic receptors.Method:We established models of hepatic encephalopathy in vivo and in vitro, the model emodin therapeutic interventions, the treatment effect was observed, while related changes observed in different models of hepatic encephalopathy in astrocytes and astrocyte such as the expression of the α7nAChRs subunits explore appropriate cellular signal transduction mechanisms. And to study the development of its occurrence during treatment correlated with hepatic encephalopathy by molecular biological methods, morphology, and pathology methods to obtain objective and detailed experimental results.Result:Experimental results show that emodin on hepatic encephalopathy has a good therapeutic effect, and the mechanism of action and astrocytes nAChRs subunits are closely related. Emodin can significantly reverse the changes in animal models of hepatic encephalopathy in liver tissue and central nervous system damage response.