| ObjectiveObserve the cytokines expression of rat hippocampus and intervention of fluoxetine in the post-stroke depression (post-stroke depression, PSD) model. Observe the intervention of fluoxetine in the expression of inflammatory cytokine and anti-inflammatory cytokine; we discuss the new mechanism of fluoxetine on antidepressant.MethodsThe healthy SD rats were randomly divided into five groups, control group, ischemia group, pure depression group, PSD group, fluoxetine treatment group.To conduct behavioral observation and testing, determination of infarct volume, measured the expression and content of TNF-α, IL-1, IL-6 in hippocampus by immunohistochemistry.ResultsCompared with the control group, hippocampus TNF-α, IL-1 levels of the other groups were increased, but the content of IL-6 decreased. With a significant statistical difference(P<0.01). HE staining showed neuronal cell damage; Compared with simple focal cerebral ischemia group: the expression of NF-κB and the content of TNF-αand IL-1 in PSD group were increased, while the content of IL-6 decreased. The difference between the two groups was significan(tP<0.01); HE staining showed significant neuronal cell damage; Compared with PSD group: different levels of fluoxetine can reduce TNF-α, IL-1 levels and increase IL-6 levels (P <0.01).ConclusionCompared with the simple stroke, PSD patients may have levels of inflammatory cytokines further increase and extend the duration of the peak, or anti-inflammatory cytokines decreased and increased in response to the delay, that is, PSD patients may have in vivo homeostasis of cytokine network. The patients under fluoxetine intervention may reduce the level of inflammatory cytokines or elevated levels of inflammatory cytokines, cytokine network to reach steady state again, improvement in symptoms of depression. It clarifies the role of fluoxetine in the treatment of depression mechanism. |