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目的:探讨芒柄花黄素(formononetin,FN)对大鼠局灶性脑缺血再灌注后炎症反应的治疗作用及其可能机制。方法:60只雄性SD大鼠随机分为假手术组、模型组、FN低中高剂量组(8、16、32 mg/kg)和尼莫地平组(12 mg/kg),每组10只,应用线栓法制作大鼠局灶性脑缺血再灌注模型,并评价其神经功能缺损情况,缺血2 h再灌注24 h后处死动物,红四氮唑(TTC)染色观察脑梗死体积的变化,并测定各组缺血区脑组织炎症因子表达,同时测定各组缺血区脑组织核转录因子-kappa B(NF-κB)和鞘氨醇激酶-1/1-磷酸鞘氨醇(Sph K1/S1P)信号通路的表达变化。结果:FN各剂量组炎症因子表达均显著降低,且NF-κB和Sph K1/S1P信号通路的激活均得到显著抑制。结论:FN对大鼠局灶性脑缺血再灌注后炎症反应保护作用机制可能与抑制Sph K1/S1P信号通路表达有关。
Objective: To investigate the therapeutic effect of formononetin (FN) on inflammatory reaction after focal cerebral ischemia-reperfusion in rats and its possible mechanism. Methods: Sixty male Sprague-Dawley rats were randomly divided into sham operation group, model group, FN low, medium and high dose groups (8,16,32 mg / kg) and nimodipine group (12 mg / kg) The model of focal cerebral ischemia-reperfusion was established by the method of thread embolization. The neurological impairment was evaluated. The animals were sacrificed 2 h after reperfusion for 24 h after ischemia, and the infarct volume was observed by TTC staining , And the expression of inflammatory cytokines in the ischemic brain tissue of each group were measured. The expressions of nuclear factor-kappa B (NF-κB) and sphingosine kinase-1 / sphingosine-1-phosphate Sph K1 / S1P) signaling pathway. Results: The expression of inflammatory cytokines in each dose group of FN was significantly decreased, and the activation of NF-κB and Sph K1 / S1P signaling pathway were significantly inhibited. CONCLUSION: FN may play a protective role in the inflammatory response after focal cerebral ischemia-reperfusion in rats, which may be related to the inhibition of Sph K1 / S1P signaling pathway.