目的 :探讨针刺对缺血性脑损伤保护作用的生化机制。方法 :采用热凝闭大鼠大脑中动脉致局灶性脑缺血模型

研究缺血 2周和 5周后缺血区皮层突触素P3 8和GAP 43的变化规律和针刺对其影响。结果 :脑缺血 2周及 5周组大鼠脑缺血区P3 8表达比假手术组显著下降 (P <0 .0 5) ;缺血 +电针 2周组与缺血 2周组相比突触素P3 8表达并无显著性差异 (P >0 .0 5) ;缺血 +电针 5周组与缺血 +电针 2周组和脑缺血 5周组相比

突触素P3 8表达明显增加 (P <0 .0 5) ;但仍明显低于假手术 5周组 (P <0 .0 5)。缺血 2周组大鼠在缺血区周围GAP 43表达与假手术组相比增加明显 (P <0 .0 5)

而缺血 5周组与假手术组相比无显著性差异 (P >0 .0 5) ;缺血 +电针 2周组大鼠脑片GAP 43表达与假手术组相比显著增加 (P <0 .0 5)

而与缺血 2周组相比无差异 (P >0 .0 5) ;缺血 +电针 5周组大鼠脑片GAP 43表达与假手术 5周组相比有显著性差异 (P <0 .0 5)。结论 :针刺可以通过提高突触素和GAP 43在缺血中心区周围皮层的表达

保护缺血性脑损伤

并可能与大脑可塑性的形成有一定的关系Objective: To explore the underlying mechanisms of acupuncture in preventing the cerebral tissue from ischemic injury. Methods: 35 SD rats were randomized into sham operation 2 week (SO 2W) group (n=6)

SO 5W group (n=6)

cerebro ischemia 2 week (CI 2W) group (n=5)

CI 5W group (n=6)

CI 2W+electroacupuncture(EA) group (n=6) and CI 5W+EA group (n=6). Cerebral ischemia model was established by middle cerebral artery heat occlusion method. EA (3～ 5 V

5～14 Hz

dense sparse waves) was applied to “Dazhui"(GV 14) for 30 min

once daily and continuously for 2 weeks. Cerebral integral neuronal synaptic vesicle membrane protein synaptophysin (P38) and growth associated protein (GAP) 43 immunoreaction of the cerebral tissue sections were displayed by using immunohistochemical technique and the immunoactivity (corrected optical density

COD) was detected by using a spectrometer system. Results: Compared with SO 2W group

COD values of P38 of CI 2W and CI 2W+EA groups were significantly lower (P<0.05); and compared with SO 5W group

P38 COD of CI 5W and CI 5W+EA groups were also significantly lower (P <0.05). Comparison between CI 2W and CI 5W groups and between CI 2W+EA and CI 5W+EA groups indicated that P38 COD values of CI 5W group and CI 5W+EA group were remarkably higher than those of CI 2W and CI 2W+EA groups separately (P<0.05)

and that of CI 5W+EA group was significantly higher than that of CI 5W group (P<0.05). Compared with SO 2W group

GAP 43 COD values of both CI 2W and CI 2W+EA groups were strikingly higher (P<0.05); and compared with SO 5W group

that of CI 5W+EA group was significantly higher. Comparison between CI 2W and CI 5W groups indicated that GAP 43 COD value of CI 5W group was remarkably lower than that of CI 2W group. No significant difference was found between CI 2W+EA and CI 5W+EA groups in GAP 43 COD values (P>0.05). It showed that after cerebral ischemia

P38 expression was downregulated markedly and GAP 43 expression upregulated

and EA could eliminate ischemia induced downregulation of P38 expression and prolong ischemia induced upregulation of GAP 43 expression. Conclusion: EA can upregulate expression of cerebral P38 and prolong the upregulation of GAP 43 expression in the cerebral ischemia rats.