川芎嗪对大鼠重型颅脑损伤后神经细胞凋亡及Bcl-2、Bax表达的影响

目的探讨川芎嗪对大鼠重型颅脑损伤后神经细胞凋亡及相关基因Bcl-2、Bax表达的影响和对脑神经的保护作用。方法120只SD健康大鼠随机分为假手术组、模型组、治疗组，其中模型组和治疗组采用Feeney自由落体撞击装置制作大鼠重型颅脑损伤模型，治疗组给予盐酸川芎嗪，用TUNEL及免疫组化法检测三组间细胞凋亡及Bcl-2、Bax蛋白的表达情况。结果大鼠脑组织中细胞凋亡率及Bcl-2、Bax表达水平在治疗组和模型明屁高于假手术组（P〈0．05）。在伤后72h、168h，治疗组的细胞凋亡率及Bax表达水平明显低于模型组，而Bcl-2的表达水平则明显高于模型组（P〈0．05）。结论川芎嗪可能通过抑制Bax的表达，上调Bcl-2的表达，减少神经细胞凋亡，减轻重型颅脑损伤后继发脑损害，从而发挥脑神经保护作用。

Effect of Ligustrazine on Apoptosis of Neurons and Expressions of Bcl-2 and Bax Genes after Severe Brain Injury in Rats

Objectives To investigate the effect of Ligustrazine（LZ） on the apoptosis of neurons, the expression of Bel-2 and Bax genes and cerebral neuroproteetion after the severe brain injury （SBI） in rats. Methods SBI model was established according to Feeney＇s method. One hundred-twenty rats were divided into 3 groups, i.e. treatment group, control group and sham injury group. The rats were treatment by imtraperitoneal injection of LZ-in the treatment group. The neuronal apoptosis and expressions of Bel-2 and Bax in the brain tissue were determined respectively by TUNEL and immunohistochemical technique in all the rats. Results The rates of TUNEL positive cells and the positive expression of Bcl-2 and Bax were significantly higher in both the treatment and control groups than those in the sham injury group （P〈0.05）. The rates of TUNEL positive cells and the positive expressions of Bax were significantly lower and the rates of the positive expression of Bcl-2 was significantly higher in the treatment group than that in the control group 72 and 68 hours after SBI （P〈0.05）. The neurological deficit score was significantly lower in the treatment group than that in the control group （P〈0.05）. Conclusions The neuronal apoptosis can be inhibited by LZ which can cause down-regulation of Bax expression and up-regulation of Bcl-2 in the rats with SBI.