CAJ | 학술논문

目的：观察缺血半暗区神经生长营养因子和抑制因子的表达变化，探讨微环境改变对神经元轴突再生、突触重建的影响。方法线栓法建立大脑中动脉栓塞(middle cerebral artery occlusion, MCAO)大鼠模型，HE染色观察脑组织病理改变；Western blot方法检测轴突再生标志蛋白生长相关蛋白-43(growth associated protein, GAP-43)及突触可塑性蛋白突触素(synaptophysin, SYN)的表达；Western blot方法检测脑源性神经营养因子(brain-derived neurotrophic factor, BDNF)、血管内皮生长因子(vascular endothelial growth factor，VEGF)、血管生成素1(angiopoietin-1, Ang1)及抑制因子NogoA(neurite outgrowth inhibitor–A)、Nogo受体(Nogo receptor, NgR)、RhoA(ras homolog gene family member A)的表达。结果大脑中动脉栓塞15 d大鼠缺血半暗区皮层神经元数目低于假手术组(P<0.01)，GAP-43表达较假手术组下调(P<0.05)，神经生长抑制因子NogoA、NogoR、RhoA表达高于假手术组(均P<0.05)；二组大鼠缺血半暗区皮层SYN及营养因子BDNF、VEGF、Ang1表达水平无明显差异(均P＞0.05)。结论神经生长抑制因子分泌增多可能与大脑中动脉栓塞导致缺血半暗区神经元轴突再生障碍发生机制相关。
목적：관찰결혈반암구신경생장영양인자화억제인자적표체변화，탐토미배경개변대신경원축돌재생、돌촉중건적영향。방법선전법건립대뇌중동맥전새(middle cerebral artery occlusion, MCAO)대서모형，HE염색관찰뇌조직병리개변；Western blot방법검측축돌재생표지단백생장상관단백-43(growth associated protein, GAP-43)급돌촉가소성단백돌촉소(synaptophysin, SYN)적표체；Western blot방법검측뇌원성신경영양인자(brain-derived neurotrophic factor, BDNF)、혈관내피생장인자(vascular endothelial growth factor，VEGF)、혈관생성소1(angiopoietin-1, Ang1)급억제인자NogoA(neurite outgrowth inhibitor–A)、Nogo수체(Nogo receptor, NgR)、RhoA(ras homolog gene family member A)적표체。결과대뇌중동맥전새15 d대서결혈반암구피층신경원수목저우가수술조(P<0.01)，GAP-43표체교가수술조하조(P<0.05)，신경생장억제인자NogoA、NogoR、RhoA표체고우가수술조(균P<0.05)；이조대서결혈반암구피층SYN급영양인자BDNF、VEGF、Ang1표체수평무명현차이(균P＞0.05)。결론신경생장억제인자분비증다가능여대뇌중동맥전새도치결혈반암구신경원축돌재생장애발생궤제상관。
Objectives To investigate the effects of nerve nutrient factors and inhibitory factors on neuronal regen? eration and axonal reconstruction at ischemic neocortical penumbra after focal cerebral ischemia in rats. Methods The rat model of middle cerebral artery ischemia was established using suture-occluded method. The pathological morpholo? gy of brain tissue was examined by using HE staining. The expression levels of GAP-43 SYN, nutrient factor (BDNF VEGF Ang1) and inhibitory factor (NogoA NogoR RhoA) were determined by using Western blotting technique. Results The number of neurons in ischemic penumbra was significantly decreased in model group (P<0.01) than in sham-operat? ed group. The expression levels of GAP-43 were significantly decreased (P<0.05) while the expression levels of NogoA NgR and RhoA in the thalamus were significantly increased (P<0.05) in model group than in sham-operated group. The expression levels of SYN and nutrient factors (BDNF VEGF Ang1) were not different between the model group and sham-operated group. Conclusion The increase in nerve inhibitory factors may contribute to the down-regulation of neu?rogenesis at ischemic neocortical penumbra after focal cerebral ischemia in rats.