Objective To observe the effect of electroacupuncture(EA)on behavior changes and the adundance levels of transforming growth factor beta 3(TGF-β3)and basic fibroblast growth factor(bFGF)proteins in the hippocampus of rats with chronic unpredictable mild stress(CUMS)-induced depression

so as to explore its mechanisms underlying improvement of depression.Methods Forty Sprague-Dawley rats were randomly divided into the following groups:control

model

EA

and medication(Fluoxetine)

n=10in each group.The depression model was established by CUMS combined with solitary raising for 28 days.EA(2Hz

0.6mA)was applied to"Baihui"(GV 20)and"Yintang"(GV 29)for 20 min

once daily before CUMS every day.The rats of the medication group were given with Fluoxetine(10mg/kg

5mL/kg)before CUMS every day.The behavioral changes(crossing and rearing locomotion)were detected by using open field tests.The expression levels of TGF-β3and bFGF proteins of the bilateral hippocampus tissues were detected using biotin label-based antibody protein chips.Results Compared to the control group

the crossed grid-square numbers and rearing times were significantly decreased in the model group(P<0.01).Following EA and medication interventions

the CUMS induced decreases of the crossed grid-square number and rearing times were notably reversed in both EA and medication groups(P<0.01)

suggesting an amelioration of depression after the intervention.The relative expression level of hippocampal TGF-β3 was down-regulated(fold change=0.48

vs the control group)and that of bFGF up-regulated(fold change=1.36

vs the control group)in the model group.In both the EA and medication groups

the down-regulated TGF-β3expression and the up-regulated bFGF protein expression were suppressed(TGF-β3:fold change=1.61

1.61 and bFGF:fold change=0.61

0.45

vs the model group respectively).Conclusion EA can improve the depression-like state in depression rats which may be associated with its effect in up-regulating hippocampal TGF-β3protein level and down-regulating bFGF protein expression via promoting neurogenesis.