丁苯酞对大鼠脑组织缺血再灌注损伤的保护作用及相关分子机制研究

摘要

Objective: To study the protective effect of butyphthalide on the cerebral ischemia-reperfusion injury in rats and the related molecular mechanism.Methods: Male SD rats were selected as the experimental animals and randomly divided into Sham group, ischemia-reperfusion group (I/R group) and butyphthalide group (NBP group), the ischemia-reperfusion models were established by suture method and then received 6 mg/kg butyphthalide sodium chloride injection before reperfusion for intervention.On 12 h, 18 h and 24 h after reperfusion, the number of apoptotic cells in brain tissue as well as the levels of cell apoptosis molecules and oxidative stress molecules were determined.Results: On 12 h, 18 h and 24 h after reperfusion, analysis of the number of apoptotic cells in brain tissue of three groups of rats was as follows: the number of apoptotic cells in brain tissue of I/R group was significantly more than that of Sham group, and the Fas, FasL, BNIP3, Caspase-3 and Caspase-9 protein expression as well as ROS and MDA levels were significantly higher than those of Sham group while CAT and SOD levels were significantly lower than those of Sham group;the number of apoptotic cells in brain tissue of NBP group was significantly less than that of I/R group, and the Fas, FasL, BNIP3, Caspase-3 and Caspase-9 protein expression as well as ROS and MDA levels were significantly lower than those of I/R group while CAT and SOD levels were significantly higher than those of I/R group.Conclusions: Butyphthalide can inhibit the apoptosis and oxidative stress reaction to reduce the cerebral ischemia-reperfusion injury in rats.%目的:研究丁苯酞对大鼠脑组织缺血再灌注损伤的保护作用及相关分子机制.方法:选择雄性SD大鼠作为实验动物并随机分为假手术组(Sham组)、缺血再灌注组(I/R组)、丁苯酞组(NBP组),采用线栓法建立缺血再灌注模型并在再灌注前给予6 mg/kg丁苯酞氯化钠注射液进行干预.再灌注后12、18、24 h时,测定脑组织中细胞凋亡的数目以及细胞凋亡分子、氧化应激分子的含量.结果:再灌注12、18、24 h时,三组大鼠脑组织中凋亡细胞数目的分析如下:I/R组大鼠脑组织中凋亡细胞的数目显著多于Sham组,Fas、FasL、BNIP3、Caspase-3、Caspase-9的蛋白表达量以及ROS、MDA的含量均显著高于Sham组,CAT、SOD的含量均显著低于Sham组;NBP组大鼠脑组织中凋亡细胞的数目显著低于I/R组,Fas、FasL、BNIP3、Caspase-3、Caspase-9的蛋白表达量以及ROS、MDA的含量均显著低于I/R组,CAT、SOD的含量均显著高于I/R组.结论:丁苯酞能够通过抑制细胞凋亡和氧化应激反应的途径来减轻大鼠脑组织缺血再灌注损伤.