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目的 研究局灶脑缺血 /再灌注大鼠蛋白激酶C(PKC)抑制剂灯盏花素缺血脑保护作用的可能机制。方法 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 4h、2 4h、72h观察PKC同工酶γ蛋白表达及神经凋亡的变化规律。结果 再灌注 4hPKCγ及神经元凋亡明显升高 ,PKCγ在 2 4h达高峰 ,72h开始下降 (P <0 .0 5 ) ;神经元凋亡的变化规律同PKCγ(P <0 .0 1) ;灯盏花素组再灌注 2 4h前能明显抑制PKCγ及神经元凋亡的表达 (P >0 .0 5 )。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。
Objective To investigate the possible protective mechanism of brain damage induced by breviscapine in rats with focal cerebral ischemia/reperfusion injury of protein kinase C (PKC). Methods Focal cerebral ischemia/reperfusion models were established by suture embolism. Changes of PKC isoenzyme γ protein expression and neuronal apoptosis were observed at 4 h, 24 h and 72 h after ischemia at 1.5 h. Results PKCγ and neuronal apoptosis were significantly increased at 4 h after reperfusion, and PKCγ peaked at 24 h and began to decrease at 72 h (P < 0.05). The neuronal apoptosis was similar to that of PKCγ (P <0.01). Breviscapine significantly inhibited the expression of PKCγ and neuronal apoptosis (P > 0.05) before reperfusion for 24 hours. Conclusion Breviscapine may be involved in ischemic brain protection and may be related to its down-regulation of PKCγ protein expression.