论文部分内容阅读
背景:肌苷参与机体多方面的代谢过程并对缺血性脑损伤有一定的保护作用,但其机制尚需做进一步研究。目的:研究大鼠缺血性脑损伤后巢蛋白(Nestin)基因表达的变化规律,探讨肌苷治疗中枢神经缺血性损伤的作用机制。设计:随机对照的基础研究。地点和材料:实验地点:青岛大学医学院脑血管病研究所和山东省脑血管病防治重点实验室完成。实验材料:成年健康雌性SD大鼠68只,以线栓法建立大脑中动脉缺血再灌注模型。随机分为治疗组和对照组,每组再随机分为缺血1.5h再灌注2,6,12,24h,2,3,7,14d组(n=4),另外4只作假手术组。干预:所有治疗均由作者亲自操作。治疗组大鼠于缺血1.5h再灌注前给予空腹注射肌苷注射液100mg/kg,2次/d。对照组大鼠同步注射相同剂量的生理盐水。所有大鼠置于同样的空间笼养。主要观察指标:应用原位杂交技术检测脑缺血再灌注后脑组织NestinmRNA的表达。结果:对照组缺血侧NestinmRNA表达皮质除2h以外、纹状体除2,6h以外、室旁区除2,6h,14d以外各时间点均明显高于假手术组。治疗组NestinmRNA表达较对照组于2,6h,7,14d在皮质,14d在纹状体有所降低,3d在皮质、纹状体及室旁区均显著升高,7d仅在纹状体、室旁区显著升高。结论:肌苷可以促进大鼠脑缺血再灌注后NestinmRNA的表达,从而达到神经组织结构和?
BACKGROUND: Inosine is involved in many aspects of the body’s metabolism and has some protective effects on ischemic brain injury. However, its mechanism needs further study. Objective: To study the changes of Nestin gene expression in rats with ischemic brain injury and to explore the mechanism of action of inosine on central nervous ischemic injury. Design: Randomized controlled basic research. Location and Materials: Experimental Location: Institute of Cerebrovascular Disease, Qingdao University School of Medicine and Shandong Provincial Key Laboratory of Cerebrovascular Disease Control completed. MATERIALS: Sixty-eight adult female Sprague-Dawley (SD) rats were used to establish a model of middle cerebral artery occlusion (MCAO). Randomly divided into treatment group and control group, each group was randomly divided into 1.5h ischemia reperfusion 2, 6, 12, 24h, 2,3,7,14 d group (n = 4), the other 4 were sham operation group. Intervention: All treatments are performed by the author himself. The rats in the treatment group were given an intraperitoneal injection of inosine 100 mg / kg twice a day for 1.5 h prior to reperfusion. Control rats were injected simultaneously with the same dose of saline. All rats were housed in the same space. MAIN OUTCOME MEASURES: Nestin mRNA expression in brain tissue after cerebral ischemia-reperfusion was detected by in situ hybridization. Results: In the control group, the expression of Nestin mRNA in the cortex was significantly higher than that in the sham-operated group at 2 h, 2 h, 14 d except 2 h except for 2 h. The expression of Nestin mRNA in the treatment group was lower than that in the control group on the cortex on the 2nd, 7th and 14th days in the cortex and on the 14th day in the striatum, while in the cortex, striatum and the paraventricular zone, Paraventricular area was significantly increased. Conclusion: Inosine can promote the expression of Nestin mRNA in rats after cerebral ischemia and reperfusion, so as to achieve the nerve tissue structure and?