目的:探究丁苯酞对缺血性脑损伤体内外保护作用及机制研究。

方法:体内实验中,将 24 只 SD 大鼠随机分为对照组、模型组、丁苯酞低剂量组、丁苯酞高剂量组,每组各6只。通过灌胃方式每日给药1次,持续1个月,使用电凝法建立永久性大脑中动脉远端闭塞动物模型,随后继续给药,直至造模后第 10 天处死,并检测相关指标。体外实验中,将神经元细胞随机分为对照组、造模组和给药组,建立缺氧缺糖/复氧复糖模型,并检测相关指标。

结果:体内实验中,造模后第 10 天时,与对照组相比,模型组神经功能评分有降低趋势,脑梗死体积较大,TNF-α 及 IL-1β 的含量均显著升高(P<0.01),TARF6 蛋白水平增高,Nrf2(Nuclear factor erythroid 2-related factor 2,Nrf2)蛋白水平显著降低,而丁苯酞高剂量组损伤得到逆转。体外实验,与对照组相比,造模组 TNF-α、IL-B、ROS 的含量显著升高,SOD 活性显著降低,TRAF6 蛋白表达升高,Nrf2 表达降低,而丁苯酞组损伤情况得到缓解。 

结论:通过抑制炎症反应和氧化应激反应，丁苯酞对缺血性脑损伤发挥保护作用。

Objective: To explore the protective effect and mechanism of butylphthalide on ischemic brain injury in vitro and in vivo.

Method: 24 SD rats were randomly divided into control group, model group, low-dose butylphthalide group, and high-dose butylphthalide group in vivo experiment, with 6 rats in each group. The drug was administered by gavage once a day for 1 month. The animal model of permanent middle cerebral artery occlusion was established by electrocoagulation, and the administration was continued until the tenth day after modeling, and detected relevant indicators. The primary neuron cells were randomly divided into control group, model group and experimental group in vitro experiment, and subsequently established a hypoxia and hypoglycemia/reoxygenation and complex glucose model, and detected related indicators

Results: In vivo experiment, on the tenth day after modeling, compared with the controlgroup, the model group had significant neurological deficits and a larger cerebral infarction volume, and the content of TNF-a and IL-1β increased significantly (P<0.01)and the level of TARF6 protein increased and Nrf2 protein decreased significantly.However, the injury in the high-dose butylphthalide group was reversed. In vitro experiment, compared with the control group, the content of TNF-a , lL-β and ROS in the model group was significantly increased, and the SOD activity was significantly decreased the TRAF6 protein expression was increased, and the Nrf2 expression was decreased. The injury in the butylphthalide group was relieved.

Conclusion: By inhibiting infammation and oxidative stress, butylphthalide plays a protective role in ischemic brain injury.