仙茅苷对局灶性脑缺血/再灌注大鼠轴突再生及Akt/GSK-3β/CRMP-2表达的影响

Curculigoside regulates Akt/GSK-3β/CRMP-2 expression and axonal regeneration in MCAO rats

目的:研究仙茅苷对局灶性脑缺血/再灌注大鼠轴突再生的作用并探讨其机制。方法:健康成年雄性SD大鼠36只,随机分为假手术组、模型对照组、仙茅苷给药组,用线栓法建立局灶性脑缺血/再灌注大鼠模型(MCAO),大鼠神经功能损伤采用Zea-Longa标准评价,Western Blot法检测大鼠缺血侧脑组织p-Akt、Akt、p-GSK-3β、GSK-3β、p-CRMP-2、CRMP-2蛋白的表达,免疫荧光染色法检测大鼠缺血侧脑组织NF200蛋白的表达。结果:与MCAO组比较,仙茅苷能明显改善大鼠的神经功能损伤,促进NF200、p-Akt、p-GSK-3β蛋白的表达,抑制p-CRMP-2蛋白表达。结论:仙茅苷能改善局灶性脑缺血/再灌注大鼠的神经功能缺损,可能通过促进Akt、GSK-3β的磷酸化,抑制CRMP-2的磷酸化,进一步促进轴突再生。

Objecyive： To investigate the axonal regeneration effect of curculigoside in MCAO rats and its potential mechanism. Methods： Thirty-six healthy adult male Sprague-Dawley rats were randomly divided into three groups： sham, MCAO, MCAO ＋ Cur groups. The rats were subjected to focal cerebral ischemia/reperfusion with suture-occluded method. Neurological deficit testing was performed with Zea Longa scale. The protein expression of p-Akt, Akt, p-GSK-3β, GSK-3β, p-CRMP-2 and CRMP-2 in side cerebral ischemic tissues were determined using Western Blot analysis. NF200 immunotluorescence staining was used to evaluate axonal regeneration. Results： Compared with MCAO group, curcuhgo- side significantly improved the neurological deficit, up-regulated the protein expression of NF200, p-Akt and p-GSK-3β, and inhibited the protein expression of p-CRMP-2. Conclusion ： Curculigoside improves neurological function recovery after focal cerebral/ischemic injury in rats, which may be associated with the up-regulation of pbesphorylated Akt and GSK-3β and inhibition of phosphorylated CRMP-2, thereby promoting axonal regeneration.