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目的观察丁苯酞对大鼠局灶性脑缺血再灌注损伤后Bcl-2蛋白表达的影响及其神经保护机制。方法 60只健康SD大鼠,制备大鼠大脑中动脉缺血再灌注模型,造模成功2 h后拔除线栓,再灌注,将造模成功的SD大鼠随机分为丁苯酞治疗组、缺血再灌注组及假手术组,每组20只。缺血再灌注组和假手术组按照150 mg/kg给予生理盐水,丁苯酞治疗组在造模后2 h以同等剂量通过腹腔注射丁苯酞注射液。各组大鼠神经功能缺损评分均在麻醉苏醒后进行;在各组中各随机选取10只大鼠,通过TTC染色观察脑梗死体积;各组余下大鼠进行免疫组化检测,观察Bcl-2蛋白表达的变化。结果三组神经功能缺损评分、脑梗死体积比较差异均具有统计学意义(P<0.05);缺血再灌注组及丁苯酞治疗组神经功能缺损评分、脑梗死体积均高/大于假手术组,差异均具有统计学意义(P<0.05)。三组Bcl-2蛋白表达阳性率比较差异具有统计学意义(P<0.05);缺血再灌注组及丁苯酞治疗组Bcl-2蛋白表达阳性率(20.12±3.36)%、(26.18±2.85)%均高于假手术组(3.15±0.42)%,差异均具有统计学意义(P<0.05);丁苯酞治疗组Bcl-2蛋白表达阳性率高于缺血再灌注组,差异具有统计学意义(P<0.05)。结论丁苯酞注射液对于大鼠缺血性脑损伤治疗有效,可以减轻大鼠脑缺血再灌注损伤的程度,具有神经保护作用,其作用机制可能与Bcl-2蛋白表达相关,并能延长缺血再灌注治疗时间窗。
Objective To observe the effect of butylphthalide on Bcl-2 protein expression and its neuroprotective mechanism after focal cerebral ischemia-reperfusion injury in rats. Methods Sixty healthy SD rats were used to establish the model of middle cerebral artery occlusion (MCAO) in rats. The rats were killed after 2 h of successful modeling and were reperfused. The successful SD rats were randomly divided into 4 groups: butylphthalide treatment group, Ischemia / reperfusion group and sham operation group, 20 rats in each group. The rats in ischemia-reperfusion group and sham operation group were treated with 150 mg / kg normal saline. Butyphthalide treatment group was given intraperitoneal injection of butylphthalide 2 h at the same dose 2 h after modeling. Neurological deficit scores of rats in each group were recovered after the anesthesia awakening. Ten rats were randomly selected in each group, and the infarct volume was observed by TTC staining. The remaining rats in each group were examined by immunohistochemistry to observe the expression of Bcl-2 Changes in protein expression. Results There were significant differences in neurological deficit score and cerebral infarction volume between the three groups (P <0.05). Neurological deficit scores and cerebral infarction volume in ischemic reperfusion group and butylphthalide treatment group were both higher than those in sham operation group , The differences were statistically significant (P <0.05). The positive rates of Bcl-2 protein in the three groups were statistically significant (P <0.05). The positive rates of Bcl-2 protein in the group of ischemia-reperfusion and butylphthalide treatment were (20.12 ± 3.36)%, (26.18 ± 2.85) )% Were significantly higher than that of the sham operation group (3.15 ± 0.42)%, the differences were statistically significant (P <0.05); the positive rate of Bcl-2 protein expression in the group of butylphthalide treatment was higher than that of ischemia-reperfusion group Significance (P <0.05). Conclusion Butylphthalide injection for the treatment of ischemic brain damage in rats, can reduce the degree of cerebral ischemia-reperfusion injury in rats with neuroprotective effect, its mechanism may be related to the expression of Bcl-2 protein, and can be extended Ischemic reperfusion treatment time window.