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目的观察梓醇对局灶脑缺血大鼠梗死灶周围大脑皮质(peri-infarction cortex,PIC)锥体神经元树突生长及突触素p38蛋白表达的影响,探讨其促脑卒中后神经修复作用及机制。方法 57只清洁级成年SD大鼠,随机分为假手术组,模型组,生理盐水组,梓醇低、中、高剂量(分别为1、5、10 mg·kg-1)组和胞磷胆碱(0.5 g·kg-1)对照组。开颅电凝右侧大脑中动脉制备局灶永久性脑缺血模型。于造模后24 h开始腹腔注射不同剂量梓醇或胞磷胆碱,每日1次,连续7d。术后1、4、7和15 d采用角落实验评估神经缺失功能恢复状况;术后1 d和15 d磁共振成像测量脑梗死体积;术后15 d,断头取脑,Golgi-Cox染色显示PIC区锥体神经元树突变化,免疫荧光组织化学染色及Western blot检测PIC区突触素p38蛋白表达。结果梓醇各剂量组和胞磷胆碱组术后7 d和15 d神经功能恢复明显优于模型组和生理盐水组(P<0.05);术后1 d、15 d,各实验组脑梗死体积差异无显著性(P>0.05);梓醇中剂量组PIC区锥体神经元树突分支数和树突棘密度均比模型组、生理盐水组和胞磷胆碱组明显增加(P<0.05);梓醇各剂量组PIC区突触素p38表达均比模型组、生理盐水组和胞磷胆碱组明显上调(P<0.05)。结论梓醇可增强局灶脑缺血大鼠PIC区锥体神经元树突可塑性,上调突触素p38表达,促进神经缺失功能恢复。
Objective To observe the effect of catalpol on dendrite growth and the expression of synaptophysin p38 protein in peri-infarction cortex (PIC) pyramidal neurons in focal cerebral ischemia rats and to explore its neurological repair after stroke Role and mechanism. Methods Fifty-seven adult SD rats of clean grade were randomly divided into sham-operation group, model group, saline group, catalpol low, medium and high dose groups (1,5 and 10 mg · kg -1) Choline (0.5 g · kg -1) control group. Cranial electrocoagulation right middle cerebral artery Preparation of focal permanent cerebral ischemia model. 24 h after model injection, different doses of catalpol or citicoline were injected intraperitoneally once daily for 7 days. At 1, 4, 7 and 15 days after operation, the nerve function recovery was evaluated by corner test. The volume of cerebral infarction was measured by magnetic resonance imaging at 1 and 15 days after operation. The brain was removed by decapitation 15 days after operation and Golgi-Cox staining was performed Dendritic changes of pyramidal neurons in the PIC region were detected by immunohistochemistry and Western blot. Results The recovery of neurological function at 7 d and 15 d after operation in catalpol group and citicoline group was significantly better than that in model group and saline group (P <0.05). On the 1st and 15th day after operation, the cerebral infarction (P> 0.05). The number of dendritic branches and dendritic spines of pyramidal neurons in the medium dose of catalpol group were significantly increased compared with the model group, the normal saline group and the citicoline group (P < 0.05). The expression of p38 synaptophysin in each dose group of catalpol was significantly higher than that in model group, normal saline group and citicoline group (P <0.05). Conclusion Catalpol can enhance the dendritic plasticity of the pyramidal neurons in the focal ischemic area of rats with focal cerebral ischemia, and upregulate the expression of p38 synaptic neurotrophic factor and promote the functional recovery of neuronal loss.