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Objective: Xiaobuxintang-2 (XBXT-2) has antidepressant effects, but the underlying mechanism is still unclear. In this study, we used the corticosterone-induced depression mouse model to study the antidepressant effect of XBXT-2and its underlying mechanisms. Methods: A mouse model of depression was induced by corticosterone. The mice were divided into 5 groups: (i) control group, (ii) corticosterone group (CORT), (iii) corticosterone + XBXT-2 (CORT + XBXT-2) group, (iv) corticosterone + XBXT-2+ lentiviral empty group (CORT + XBXT-2 + no-load), (v) corticosterone + XBXT-2+ lentivirus GSK3β Overexpression group (CORT + XBXT-2 + GSK3β). The expression level of GSK3β in the hippocampus was detected by immunoblotting, and the depression status of the mice was evaluated by forced swimming test and tail suspension test. Results: The GSK3β lentivirus induced the high expression of GSK3β in the hippocampus of mice, and the mRNA and protein levels were significantly increased compared with the control group. The immobility time is significantly increased in corticosterone injection-induced depression model mice (CORT group), and XBXT-2 can effectively reduce the immobility time of depression model mice. Overexpression of GFP empty lentivirus did not affect mouse behavior, whereas overexpression of GSK3β significantly increased immobility time in depression model mice according to forced swimming and tail suspension experiments. Conclusion: High expression of GSK3β in the hippocampus of mice can inhibit the therapeutic effect of XBXT-2 on the corticosterone-induced depression in mice