Abstract
group, model+EA group, and model+fluoxetine group. Use biotin-labeled protein chip technology to detect the protein expression of TGF3, FS L-1 and IL-1 of hippocampus. Results:Compared to the control group, the protein expression of TGF3 in the model group were down-regulated (fold change= 0.48), FSL-1 and IL-1 were up-regulated (fold change=1.27; 1.57). Compared to the model group, the protein expression of TGF3were up-regulating in themodel+EA group (fold change=1.61) and the model+fluoxetine group (fold change=1.60), while the protein expression of FSL-1 and IL-1 were both down-regulating in the model+EA group (fold change=0.75; 0.60) and the model+fluoxetine group (fold change=0.67; 0.54). Conclusion: The results showed that EA improved significantly dysfunction of hippocampus by facilitating hippocampal neuron differentiation and preventing them apoptosis and inflammation, which was as effective as fluoxetine. Consequently, EA is a useful antidepressant treatment for depression model rats. Contact: Xuhui Zhang, rabbit zxh@163.com
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