RÉSUMÉ
Objective To investigate whether salvianolic acid B(Sal B)can improve the cognitive function in rats with post-traumatic stress disorder(PTSD)by regulating GSK-3β/β-Catenin signal pathway.Methods Sixty rats were randomly grouped into the normal group,the PTSD group,the Sal B low-dose group(10 mg/kg),the Sal B high-dose group(20 mg/kg)and the GSK-3β inhibitor group(30 mg/kg CHIR-99021),with 12 rats in each group.In addition to the normal group,rats in other groups were constructed PTSD rat models by using single prolonged stress(SPS)method.Open field test and Morris water maze test were applied to evaluate the cognitive function of rats.Nissl staining was applied to observe the pathological changes of hippocampal neurons.TUNEL staining was applied to detect the apoptosis of hippocampal neurons.Western blot assay was applied to detect the expression of cleared caspase-3,B-cell lymphoma gene-2-associated X protein(Bax),proto-oncogene(c-Myc),Cyclin D1,total GSK-3β(t-GSK-3β),phosphorylated GSK-3β(p-GSK-3β),total β-Catenin(t-β-Catenin)and phosphorylated β-catenin(p-β-Catenin)proteins in hippocampus.Results Compared with the PTSD group,the number of crawling spaces,standing times,total movement distance and times of crossing the original platform of rats were higher in the Sal B low-dose group,the Sal B high-dose group and the GSK-3β inhibitor group.The escape latency and the time to cross the original platform for the first time were shorter,the apoptosis rate of hippocampal neurons and the expression levels of Bax,cleaved caspase-3,t-GSK-3β and p-β-Catenin proteins in hippocampus were lower,and the expression levels of Cyclin D1,c-Myc,p-GSK-3β,t-β-Catenin proteins were higher(P＜0.05).Conclusion Sal B can reduce the apoptosis and damage of hippocampal neurons in rats with PTSD and improve cognitive dysfunction in rats,and inhibit the GSK-3β/β-Catenin signal pathway.