利多卡因对大鼠缺血脑损伤后海马CA1区神经元凋亡及细胞色素C释放的影响

Effect of lidocaine on neuronal apoptosis and cytochrome C release in hippocampal CA1 subregion of rat brain after ischemic injury

目的:观察利多卡因对大鼠缺血脑损伤后海马CA1区神经元凋亡的影响。方法:雄性SD大鼠,随机分成假手术组、模型组(制作缺血脑损伤模型)、利多卡因治疗组,每组10只。手术后24h分离右侧海马组织。TUNEL法检测3组大鼠海马CA1区细胞凋亡,免疫组化染色测定细胞色素C(CytC)蛋白和Bax蛋白的表达。结果:①与对照组相比模型组凋亡细胞数明显增加,与模型组相比治疗组凋亡细胞数明显降低(P均<0.001)。②与对照组相比,模型组CytC阳性细胞数明显减少,Bax蛋白阳性细胞数明显增多(P<0.001);与模型组相比,治疗组CytC阳性细胞数明显增加,Bax蛋白阳性细胞数明显下降(P<0.001)。结论:利多卡因可减少脑缺血后海马CA1区神经元CytC的释放并降低Bax蛋白的表达,对海马CA1区神经元有保护作用。

Aim ： To observe the effect of lidocaine on neuronal apoptosis in hippocampal CA1 of rat brain after ischemic injury. Methods： Thirty male SD rats were randomly allocated into sham-operation group, model group （ischemic injury） , and treatment group （ ischemic injury ＋ lidocanine） , 10 rats in each group. The right hippocampus was isolated 24 h after ischemic injury. TUNEL was used to measure the neuron apoptosis. Immunochemistry was adopted to detect the expression of cytochrome C and Bax protein. Results： The rate of apoptosis neurons in model group was significantly higher than that in sham-operation group （P 〈 0.001 ）, and the rate of apoptosis neurons in treatment group was significantly lower than that in model group （P 〈 0. 001 ） ; the number of cytochrome C-positive neurons in model group decreased and Bax-positive neurons increased compared with sham-operation group （P 〈 0. 001 ） ; the number of Cyt C-positive neurons in treatment group was significantly increased and that of Bax-positive neurons decreased compared with model group （P 〈 0. 001 ）. Conclusion ： Lidocaine can inhibit cytochrome C release into cytoplasm and reduce the expression of Bax in neurons of hippocampal CA1. Lidocaine could inhibit the apoptosis of neurons in hippocampal CA1.