三七总皂苷对脑缺血再灌注大鼠神经血管单元超微结构的影响

Effects of Panax notoginseng Saponins on Ultrastructure of Neurovascular Units in Rats with Cerebral Ischemia Reperfusion

为了观察脑缺血再灌注(cerebral ischemia reperfusion, CIR)大鼠缺血灶周边脑组织不同时间点神经血管单元(neurovascular unit, NVU)超微结构变化,研究三七总皂苷(Panax notoginseng saponins, PNS)对脑缺血再灌注大鼠脑组织NVU超微结构的影响,本研究采用改良Zea Longa法制作局灶性大脑中动脉闭塞(MCAO)模型,缺血2 h后再灌注;采用Longa法评分标准检测各组大鼠术后4 h神经功能评分,随之各组进行干预,分别在缺血再灌注后24 h、72 h、7 d、3周进行神经功能评分和透射电镜下观察各组大鼠缺血灶周边脑组织的NVU超微结构变化。研究结果表明,干预前即术后4 h治疗组和对照组神经功能评分比较无明显差异;PNS干预后治疗组大鼠神经功能评分逐渐改善,缺血再灌注后24 h与对照组比较,差异无统计学意义(p>0.05),再灌注72 h、7 d、3周的大鼠神经缺损评分与同时间点对照组相比差异具有统计学意义(p<0.05)。电镜观察发现再灌注24 h、72 h、7 d、3周治疗组大鼠脑组织NVU超微结构的病理形态损伤均较同时间点对照组明显减轻。本研究结论认为,PNS通过整合促进脑缺血后NVU的神经元、胶质细胞和微血管的修复,改善神经功能缺损症状,对脑缺血具有保护作用。

To observe the ultrastructural changes of neurovascular unit(NVU) in peripheral brain tissue around ischemic lesion of cerebral ischemia reperfusion(CIR) rats at different time points, the effect of Panax notoginseng saponins(PNS) on NVU ultrastructural changes in cerebral tissue of cerebral ischemia reperfusion rats was studied. In this study, the modified Zea Longa method was used to establish a focal middle cerebral artery occlusion(MCAO) model, and reperfusion was performed after 2 h of ischemia. The neurological function scores of the rats in each group were detected by Longa scoring criteria 4 h after surgery, and then the intervention was carried out in each group. Neurological function scores were performed 24 h, 72 h, 7 d and 3 weeks after ischemia reperfusion respectively, and the NVU ultrastructural changes of the cerebral tissues around the ischemic focus in each group were observed under transmission electron microscope. The results showed that there was no significant difference in neurological function scores between the treatment group and the control group before and4 h after the intervention. The neurological function score of rats in the PNS intervention group was gradually improved, and the difference was not statistically signific ant 24 h after ischemia reperfusion compared with the control group(p>0.05). The neurological defect score of rats in the reperfusion group at 72 h, 7 d, and 3 weeks was statistically significant compared with the control group at the same time point(p<0.05). The pathological morphological damage of NVU ultrastructure in rats treated with reperfusion at 24 h, 72 h, 7 d and 3 w was significantly reduced compared with that in the control group at the same time point. Our study concluded that PNS could promote the repair of NVU neurons, glial cells and microvessels after cerebral ischemia, improve the symptoms of neural function defects, and have a protective effect on cerebral ischemia.