Effects Of Propofol Treatment On Expression Of JAK-ARAT Pathway And Cell Apoptosis In Brain Tissue In Rats With Lps-induced Brain Injury

Objective: To investigate neuroprotective effects of Propofol on theexpression of P-JAK2、P-STAT3and cell apoptosis in brain tissue in ratswith LPS-induced brain injury and the possible mechanism.Methods: Seventy two male and female SD rats weighting220-250gwere randomly divided into3groups(n=24each):Cerebral edema wasinduced by injecting LPS1mg/kg via left internal carotid artery in group Land group LP.In C group,equal volume of nomad saline was administeredinstead of LPS.Group LP received intraperitoneal Propofol100mg/kgimmediately after LPS administration.Six rats of each group weredecapitated at6h、12h、24h and48h after operation and their frontal lobecortex were immediately removed for determination of water content. Theexpression of the apoptotic neurons were detected by Annexin V-PI, theexpression of P-JAK2、P-STAT3、NF-κB、AIF and Caspase-3proteins weredetected by immunohistochemistry,and the Western blot analysis were usedto detect the expression of P-JAK2、 P-STAT3and NF-κB proteins.Pathological change in brain was observed with light microscope.Results: The brain water content、the number of neuronal apoptosisincreased，the expression of P-JAK2、P-STAT3、NF-κB、AIF and Caspase-3proteins were significantly increased in group L and group LP comparedwith group C (P <0.05, P <0.01).In group LP these results weremarkedly reduce compared with group L (P <0.05, P <0.01).Themicroscopic examination showed that brain injury was attenuated in groupLP compared with group L.Conclusion:(1) LPS can induce brain injury and cell apoptosis，whichmay be correlated with upregulation the expression of P-JAK2、P-STAT3and NF-κB，activated JAK/STAT signal pathway may involved in thedevelopment process;(2) Propofol can attenuate LPS-induced brain injurymight be related to the decrease of P-JAK2、P-STAT3and NF-κB proteinexpression and the inhibition of apoptosis， thereby reduced theinflammatory response.