厚朴酚对大鼠脑创伤后神经元凋亡及死亡相关蛋白激酶表达的影响

Effects of Magnolol on death associated protein kinase expression and neuron apoptosis following traumatic brain injury in mice

目的观察厚朴酚对大鼠脑创伤后神经细胞死亡相关蛋白激酶（DAPK）的表达和凋亡的影响，探讨厚朴酚对脑创伤后神经细胞凋亡的脑保护机制。方法建立大鼠自由落体脑创伤模型，雄性的Wister大鼠60只，随机数字表法分为脑损伤组、生理盐水组、脂肪乳剂组、厚朴酚组各4组15只。采用TUNEL法观察细胞凋亡和RT—PCR法观察DAPKmRNA在脑创伤后的变化。结果脑创伤后受伤区、受伤周边区神经细胞过度表达DAPKmRNA，并且出现明显的神经细胞凋亡，厚朴酚能够使DAPKmRNA的表达高峰及神经细胞凋亡高峰下调。结论厚朴酚可能通过抑制DAPK的表达，减少神经细胞凋亡而发挥脑保护作用。

Objective To observe the effects of magnolol on death associated protein kinase （DAPK） expression and neuron apoptosis after traumatic brain injury （TBI） in mice. Methods Models of TBI rats were established by free drop impact mode. These 60 adult rats weighed 250 ~ 300g were randomly divided into TB｜ groups, NS group, fat emulsion group and magnolol（2 mg/kg ~ h, iv pump）group, with 15 rats each. Using RT- PCR method to determine the expression of DAPK mRNA. TUNEL method was applied to determine neuron apoptosis. Results The expression of DAPKmRNA and apoptosis myocytes significantly increased in brain injury groups （P 〈 0.05 ）. The expression of DAPKmRNA and apoptosis myocytes in rats with magnolol （2 mg/kg · h, iv pump） decerased significantly than other groups （P 〈 0. 05）. Conclusion DAPK is activated in neuron of rats after TBI. The suppression of the expression of DAPKmRNA in models of TBI rats is probably related to protective effect of magnolol on TBI.