Tetrandrine Inhibits Apoptosis Signaling Pathway Via Reducing TRAF1 To Improve TBI

Objective: The aim of study is to explore the therapeutic effect of Tet in traumatic brain injury(TBI)and its endogenous mechanism.Methods: First,surface plasma resonance(SPR)was adopted to determine the affinity of Tet and TRAF1.The models for scratch injury of astrocytes(AST)in vitro and craniocerebral impact injury of rats in vivo were established.Then,animal behavior score was uesd to evaluat the neurological function of rats.HE staining and TUNEL assay was employed to determine the pathological state and the cell apoptosis.The expression of TRAF1 was detected by using immunofluorescence staining,flow cytometry determined the cell apoptosis,and western blot was employed to measure the expression levels of TRAF1,AKT,p-AKT,Bax,Bcl-2.Results: The results of SPR indicated that Tet and TRAF1 had a good degree of docking anastomosis.In the AST scratch injury model,AST apoptosis was reduced,and the cellular activity was significantly improved after Tet intervention.In the rat model with TBI,we observed a significant improvement in animal behavior after Tet intervention.HE staining indicated that the degree of pathological injury of brain tissue was reduced,and TUNEL staining revealed that the rate of apoptosis was significantly reduced.In both groups of models,we observed that the expression of TRAF1 and p-Akt/Akt was downregulated after Tet intervention,whereas the expression of Bcl-2/Bax was upregulated.Further upregulation of TRAF1 expression could reverse this effect.Conclusion: 1.Tet may be a suitable candidate drug for TBI treatment.2.The therapeutic effect of Tet on TBI may be related to the regulation of the TRAF1/Akt/Bax signaling pathway to inhibit cell apoptosis.