Objective:To explore the effects and anti-depression mechanisms of Kaixin Jieyu Decoction(开心解郁汤,KJD).Methods:The rat vascular depression(VD) model was established by ligation of bilateral common carotid arteries(LBCCA) combined with chronic unpredictable mild stress(CUMS).Forty Wistar rats were randomly divided into sham,VD model,VD + high-dose KJD[15.4 g/(kg·d) of crude drug],VD + medium-dose KJD[7.7 g/(kg·d) of crude drug],and VD + fluoxetine[2.4 mg/(kg·d)]groups(r>=8 in each group),and the treatments lasted for 21 days.Changes of behavior and hippocampus pathology were observed.The level of glial fibrillary acidic protein(GFAP)protein and mRNA in hippocampus was detected respectively by immunohistochemistry and real-time polymerase chain reaction.Results:Compared with the sham group,rats in model group showed a variety of behavioral obstacles,including a significant reduction in sucrose consumption percentage,horizontal and vertical activity scores in open-field tests(P<0.05 or P<0.01),pathological damage like neuronal degeneration,necrosis,and a significant decrease of GFAP protein and mRNA in hippocampus(P<0.01);compared with the model group,rats in the high-dose KJD group,medium-dose KJD group and fluoxetine group obtained notable higher behavioral scores,and pathological injury lessened in hippocampus with a increased expression of GFAP protein and mRNA(P<0.05 or P<0.01);compared with the medium-dose KJD group and fluoxetine group,GFAP mRNA in highdose KJD group expressed higer(P<0.05).Conclusion:LBCCA combined with CUMS may cause depression-like behavioral changes resulting in the VD model of rats whose depression state can be ameliorated by KJD,and the mechanism of cerebral protection is related possibly with promoting expression of GFAP in hippocampus. Objective: To explore the effects and anti-depression mechanisms of Kaixin Jieyu Decoction. Methods: The rat vascular depression (VD) model was established by ligation of bilateral common carotid arteries (LBCCA) combined with chronic unpredictable mild stress (CUMS) .Forty Wistar rats were equally divided into sham, VD model, VD + high-dose KJD [15.4 g / (kg · d) of crude drug], VD + medium- dose KJD [7.7 g / (kg · D) of crude drug], and VD + fluoxetine [2.4 mg / (kg · d)] groups (r> = 8 in each group), and the treatments lasted for 21 days. Changes in behavior and hippocampus pathology were observed. The level of glial fibrillary acidic protein (GFAP) protein and mRNA in hippocampus was detected respectively by immunohistochemistry and real-time polymerase chain reaction. Results: Compared with the sham group, rats in model group showed a variety of behavioral obstacles, including a significant reduction in sucrose consumption percentage, horizontal and vertical activity scores in open-field tests (P <0.05 or P <0.01), pathological damage like neuronal degeneration, necrosis, and a significant decrease of GFAP protein and mRNA in hippocampus (P <0.01); compared with the model group, rats in the high-dose KJD group, medium- dose KJD group and fluoxetine group obtained not higher behavior scores, and pathological injury lessened in hippocampus with a increased expression of GFAP protein and mRNA (P <0.05 or P <0.01); compared with the medium-dose KJD group and fluoxetine group, GFAP mRNA in high dose KJD group expressed higer (P <0.05) .Conclusion: LBCCA combined with CUMS may cause depression-like behavioral changes resulting in the VD model of rats who depression state can be ameliorated by KJD, and the mechanism of cerebral protection is related possibly with promoting expression of GFAP in hippocampus.