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目的探讨神经调节素(NRG-1β)对大鼠脑缺血损伤的预防性治疗作用和机制。方法Wistar大鼠150只,应用线栓法建立大鼠大脑中动脉闭塞(MCAO)模型,随机分为对照组和治疗组,在MCAO前经颈内动脉注射NRG-1β(2μg/kg)进行预防性治疗。在MCAO后0 h、0.5 h、1.0 h、1.5 h和2.0 h分别用干湿重法测定脑组织含水量,氯化三苯基四氮唑(TTC)染色测定脑梗塞体积,细胞凋亡用末端脱氧核苷酸转移酶介导的生物素脱氧尿嘧啶核苷酸缺口末端标记(TUNEL)法,早期生长反应基因-1(Egr-1)表达水平用免疫组化检测。结果大脑中动脉阻断后,动物脑组织含水量和梗塞面积随着缺血时间的延长而逐渐增加,NRG预处理组脑组织含水量低于对照组,梗塞范围也明显缩小。脑缺血可诱导脑组织细胞凋亡和Egr-1表达,随着缺血时间的延长,凋亡细胞和Egr-1阳性细胞数明显增多;NRG颅处理能明显减少缺血诱导的细胞凋亡数,增加Egr-1的表达水平.结论NRG-1β可能通过抑制凋亡途径和诱导Egr-1表达水平,对缺血性脑损伤具有积极的保护作用。
Objective To investigate the preventive effect of neurotensin (NRG-1β) on cerebral ischemic injury in rats and its mechanism. Methods A total of 150 Wistar rats were divided into control group and treatment group by thread occlusion. MCAO model was established by intracarotid injection of NRG-1β (2μg / kg) before MCAO Sexual treatment. The water content of brain tissue was measured by dry-wet weight method at 0 h, 0.5 h, 1.0 h, 1.5 h and 2.0 h after MCAO, and the infarction volume and apoptosis were measured by TTC staining Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and early expression of Egr-1 were detected by immunohistochemistry. Results After occlusion of the middle cerebral artery, the water content and the infarction area of the brain tissue gradually increased with the prolongation of the ischemic time. The water content of brain tissue in the NRG preconditioning group was lower than that in the control group, and the infarct size was also significantly reduced. Cerebral ischemia induced apoptosis of brain cells and expression of Egr-1. With the prolongation of ischemia, the number of apoptotic cells and Egr-1 positive cells increased obviously. NRG treatment significantly reduced the apoptosis induced by ischemia And increase the expression level of Egr-1.Conclusion NRG-1β may have a protective effect on ischemic brain injury by inhibiting the apoptosis pathway and inducing Egr-1 expression.