西酞普兰通过免疫调节机制治疗脑卒中后抑郁状态

目的本研究通过观察脑卒中后抑郁(post stroke depression,PSD)大鼠给予抗抑郁药物西酞普兰干预后,观察下丘脑TNF-α的表达变化,并探讨PSD发病机制和潜在的药物治疗机制。方法经旷场实验筛选出18只大鼠,随机分为对照组6只,另12只大鼠经过单侧大脑中动脉线栓法后,又随机分为PSD组6只和西酞普兰组6只,经慢性不可预见性应激后,通过旷场实验和糖水实验观察各组大鼠的行为学改变,定量PCR检测各组大鼠下丘脑TNF-αmRNA的表达改变。结果与对照组比较,PSD组的水平活动、直立探索和糖水喜好明显下降,差异有统计学意义(P<0.01);西酞普兰组的水平活动、直立探索和糖水喜好较PSD组明显升高,差异有统计学意义(P<0.05)。PSD组下丘脑TNF-αmRNA水平较对照组明显升高,差异有统计学意义(P<0.05);西酞普兰组下丘脑TNF-αmRNA水平较PSD组明显下降,差异有统计学意义(P<0.05)。结论抗抑郁药物西酞普兰可通过调节下丘脑TNF-α治疗PSD。

Citalopram in treatment of post stroke depression through its immunoregulatory mechanism

Objective To study the expression of TNFα in hypothalamus of rats by observing post stroke depression and its pathogenesis after citalopram treatment.Methods Eighteen rats that underwent open field test were randomly divided into the control group(n=6) and experimental group(n=12).The rats in experimental group were further divided into post stroke depression group(n=6) and citalopram treatment group(n=6) after left middle cerebral artery occlusion.Behaviors in these two groups were observed by open field test and sugar-water test,respectively.Expression of TNF-α mRNA in hypothalamus of rats was detected by quantitative polymerase dhain reaction.Results The levels of horizontal and vertical activities and the preference for sugar-water were significantly lower in post stroke depression group than in control group(P<0.01) and significantly higher in citalopram treatment group than in post stroke depression group(P<0.05).The TNF-α mRNA expression level in hypothalamus was significantly higher in post stroke depression group than in control group(P<0.05) and significantly lower in post stroke depression group than in citalopram treatment group(P<0.05).Conclusion Citalopram exerts its therapeutic effect on post stroke depression by down-regulating the expression of TNF-α in hypothalamus of rats.