NAD^+对tMCAO小鼠的脑保护作用

Treatment of NAD^+ protects transient middle cerebral artery occlusion in the mouse model of tMCAO

目的探讨烟酰胺腺嘌呤二核苷酸(NAD+)对大脑中动脉短暂阻塞再灌注(tMCAO)小鼠的脑保护作用。方法实验分为正常组、假手术组,缺血2 h再灌注模型组和烟酰胺腺嘌呤二核苷酸组;采用线栓法制作tMCAO小鼠模型;2 h后再灌注时立即腹腔注射NAD^+建立tMCAO+NAD^+组;48 h后观察以上4组小鼠行为学的差异,采用苏木素-伊红(HE)染色法对小鼠脑组织进行染色,观察其病理变化及计算梗死体积,利用尼氏染色法检测尼氏小体的变化。结果与正常组及假手术组相比较,tMCAO组出现明显神经损伤性异常行为;tMCAO组脑组织出现严重病理变化,脑梗死体积增大,单位体积脑组织内神经细胞数量减少,尼氏小体减少。tMCAO+NAD^+组与tMCAO组比较,神经功能缺损程度明显减轻(P<0.05),梗死体积减小(P<0.01),单位体积脑组织内神经细胞数量多,尼氏小体多。结论 NAD^+对tMCAO小鼠的脑损伤有一定的保护作用。

ObjectiveTo explore the effect of NAD^＋treatment for AIS in the mouse model of transient focal brain ischemia（tMCAO）.Methods Animals was divided into control group, sham group, tMCAO group and tMCAO＋NAD^＋ group. tMCAO model was generated by nylon suture method. We built the tMCAO＋NAD^＋ group by the intra-peritoneal injection NAD^＋ 50 mg/kg immediately after reperfusion. The behaviour was quantified 48hours later. HE-staining was performed to compared pathological changes and infarct volumes by, meanwhile, nissl staining was used to detect the Nissl changes.Results Compare to the sham group, 48hours after ischemia, severe damages were determined in tMCAO group, including pathological changes, increasing infarct volumes, decreaseing of neurones and Nissl signals. compared to the the tMCAO group,the tMCAO＋NAD^＋group had significant decreases of infarct volumes（P〈0.01）, less neurological deficits（P〈0.05）and more neurones and the Nissl signals.Conclusion Our study indicated the protective effort of NAD^＋ for brain after transient middle cerebral artery occlusion.