阿魏酸对脑梗死大鼠的神经功能、GLUT蛋白与神经元葡萄糖代谢的影响

目的 探究阿魏酸在减轻大鼠脑梗死过程中对葡萄糖转运蛋白（GLUTs）和神经元葡萄糖代谢的影响。方法 72只SD大鼠随机分为假手术组、模型组、尼莫地平组以及阿魏酸25、50、100 mg/kg组。采用Longa线栓法构建脑梗死模型，梗死期间，模型组尾iv生理盐水，阿魏酸组分别尾iv 25、50、100 mg/kg的阿魏酸治疗，尼莫地平组尾iv 20 mg/kg尼莫地平，给药3 d。完成给药后24 h，对各组大鼠开展神经功能评分，完成后取大鼠血液检测外周血糖值，再通过PET/CT实验检测缺血区葡萄糖摄取水平。将大鼠处死后全脑组织进行TTC染色，取缺血核心区组织，通过比色法检测ATP含量，采用Western blotting法检测GLUT蛋白表达水平。结果 与假手术组比较，模型组大鼠神经功能评分增加，出现明显梗死区域，缺血核心区葡萄糖摄取量减少，ATP含量降低，GLUT1、GLUT3、PFKFB3蛋白表达降低（P＜0.05）。与模型组比较，阿魏酸50、100 mg/kg组大鼠神经功能评分减少，梗死区域面积占比减少，缺血核心区葡萄糖摄取量增加，ATP含量升高，GLUT1、GLUT3、PFKFB3蛋白表达升高（P＜0.05）。结论 阿魏酸对脑梗死大鼠的治疗效果与尼莫地平相似，其机制可能与提高GLUT1和GLUT3蛋白表达，促进葡萄糖向中枢神经元转运，提高葡萄糖代谢相关。

Effects of ferulic acid on neurological function, GLUT protein, and neuronal glucose metabolism in rats with cerebral infarction

Objective To explore the effects of ferulic acid on glucose metabolism and GLUTamic acid in rats with cerebral infarction. Methods 72 SD rats were randomly divided into sham operation group, model group, nimodipine group, ferulic acid 25, 50, 100 mg/kg group. The cerebral infarction model was constructed by Longa line embolus method. During the infarction, the model group was treated with tail iv normal saline, ferulic acid group with tail iv of 25, 50, and 100 mg/kg respectively, and the nimodipine group with tail iv of 20 mg/kg nimodipine, the drug was administered for 3 d. 24 h after the administration of the drug, the rats in each group were collected to carry out neurological function scores. After the completion of the treatment, the blood of the rats was collected to detect peripheral blood sugar value, and then the glucose uptake level in the ischemic area was detected by PET/CT experiment. After the rats were killed, the whole brain tissues were stained with TTC, the ischemic core tissues were taken, ATP content was detected by colorimetry, and GLUTprotein expression level was detected by Western blotting experiment. Results Compared with the sham operation group, the neurological function score of the model group was increased, the infarction area was obvious, the glucose intake in the ischemic core area was decreased, and the ATP content was decreased (P < 0.05). The expression levels of GLUT1, GLUT3, and PFKFB3 protein were decreased (P < 0.05). Compared with the model group, the neurological function score was decreased, the percentage of infarction area was decreased, the glucose intake in the ischemic core area was increased, and the ATP content was increased in the ferulate acid 50 and 100 mg/kg group (P < 0.05). The expression of GLUT1, GLUT3, and PFKFB3 protein were increased (P < 0.05). Conclusions The therapeutic effect of ferulic acid on ischemic stroke rats is similar to nimodipine, and its mechanism may be related to increasing the expression of GLUT1 and GLUT3 protein, promoting the transport of glucose to central neurons, and improving glucose metabolism.