Ammonia Acts On Astrocytes To Cause Brain Edema By Up-regulating The P-Erk_1/2 Pathway And Causing An Increase In Aquaporin 4 Expression

ObjectiveTo discuss the successive expression of P-Erk_1/2 pathway and aquaporin 4after cerebral edema induced by ammonia.MethodsThe experiment divided 60 mice into 2 groups:blank control group?Blank Group,n=10?,urease group?Urease,n=50?,Urease component was injected intraperitoneally every day for 5 periods?33 U/kg?,the blank group was intraperitoneally injected with the same amount of normal saline.The first group was injected with urease for 6 hours,and then the brain was decapitated after chloral hydrate anesthesia.The second group,the brain was decapitated 6hours after the injection of urease continued on the second day and the other three groups are similar.Western blot was used to detect the expression of aquaporin 4?AQP4?,and the highest time point of AQP4 expression was selected for brain stem wet weight measurement.The newly born suckling mice within 24 hours were taken out of the brain by decapitation,cut and digested,and then after being cultured for one month in the dishes for MTT,Western Blot and immunofluorescence,which were used to detect cell proliferation and expression of related proteins such as AQP4 and P-Erk_1/2.ResultsAfter the hyperammonia model was established by injecting urease,it was found that the AQP4 of brain edema related protein increased most significantly on the second day?P<0.01?,and the wet weight of brain stem was also higher than that of the control group?P<0.05?.MTT cell proliferation assay showed that the concentration of ammonium chloride did not cause the death of astrocytes at 5mM,but some micro-stimulative effects were observed?P<0.01?.Ammonia-treated astrocytes increased P-Erk_1/2 expression at 2 hours,followed by increased AQP4 expression at 24 hours,and immunofluorescence further confirmed an increase in AQP4 expression during ammonia treatment for 24hours.ConclusionsAfter ammonia treatment of astrocyte,it first passes through the P-Erk_1/2pathway,which in turn causes an increase in AQP4 expression,and finally leads to cerebral edema.