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背景:蛋白激酶C(ProteinKinaseC,PKC)抑制剂能明显减轻缺血性脑损害,但其毒副作用大、价格昂贵。灯盏花素注射液能明显抑制PKC活性,对缺血性脑损害有一定的保护作用。目的:研究局灶脑缺血再灌注大鼠PKC抑制剂灯盏花素缺血脑保护作用的可能机制。设计:完全随机设计,对照实验研究。主要观察指标:采用线栓法制备大鼠局灶脑缺血再灌注模型。于缺血1.5h再灌注4,24,72h观察PKC同工酶γ蛋白表达及神经元凋亡的变化规律。结果:再灌注4hPKCγ及神经元凋亡明显升高,PKCγ在24h达高峰,72h开始下降(P<0.05);神经元凋亡的变化规律同PKCγ(P<0.01);灯盏花素组再灌注24h前能明显抑制PKCγ及神经元凋亡的表达(P>0.05)。结论:灯盏花素的缺血脑保护作用可能与其下调PKCγ蛋白表达有关。
BACKGROUND: Protein kinase C (PKC) inhibitors can significantly reduce ischemic brain damage, but their side effects are high and expensive. Breviscapine injection can significantly inhibit PKC activity, has a certain protective effect on ischemic brain damage. Objective: To investigate the possible mechanism of cerebral protection of breviscapine in ischemic brain by focal PKC inhibitor of focal cerebral ischemia-reperfusion in rats. Design: Completely randomized design, controlled experimental study. MAIN OUTCOME MEASURES: A rat model of focal cerebral ischemia-reperfusion was established by thread occlusion. The changes of PKC isoenzyme-γ protein expression and neuronal apoptosis were observed at 4h, 24h and 72h after reperfusion for 1.5h after ischemia. Results: After 4h of reperfusion, the apoptosis of PKCγ and neurons was significantly increased, the peak of PKCγ reached the peak at 24h, and then decreased at 72h (P <0.05). The change of neuronal apoptosis was similar to that of PKCγ (P <0.01) 24h before can significantly inhibit the expression of PKCγ and neuronal apoptosis (P> 0.05). Conclusion: The protective effect of breviscapine on ischemic brain may be related to its downregulation of PKCγ protein expression.