c—fos反义寡聚核苷酸对脑缺血性损伤和电针抗损伤作用的影响

用c-fos反义寡聚核苷酸脑内微量注射、TTC染色、c-Fos免疫组织化学和电针等技术和方法，探讨即早反应基因c-fos在大鼠局灶性脑缺血（MCAO）模型的脑损伤中和电针抗局灶性脑缺血脑损伤中所起的作用。实验结果表明，局灶性脑缺血可引起c-fos在缺血侧皮质的大量表达，电针能部分抑制这种表达，使脑缺血梗死灶体积减小。在缺血中心区注射c-fos反义寡聚核苷酸后，脑内c-fos的表达基本上被完全阻断，导致脑梗死灶的体积明显增大，电针抗脑缺血脑损伤的作用也被取消，提示脑缺血后，脑内的c-fos适度表达可能对脑损伤有一定的保护作用。电针可能部分抑制了脑内c-fos表达，调整了缺血后的c-fos表达的程度，对脑缺血损伤起一定的保护作用。

Effect of c-fos antisense oligodeoxyneucleotide on injury of transient focal cerebral ischemia and acupuncture anti-injury of brain focal ischemia

Brain microinjection of c-fos antisense oligodeoxyneucleotide (c-fos antisense), TTC staining, c-Fos immunohistochemistry and electroacupuncture (EA) were adopted for probing the effects of c-fos antisense on the brain injury induced by transient focal cerebral ischemia and EA anti-injury of brain ischemia in rat model with middle cerebral artery occlusion (MCAO). The results show that focal cerebral ischemia can induce the expression of c-fos in the cerebral cortex of ischemic side and EA can inhibit part of c-Fos expression resulting in reducing the volume of brain infarct. After microinjection of c-fos antisense into the central area of cerebral ischemia the expression of c-fos was nearly depressed and the volume of brain ischemic infarct was increased,at the same time the anti-injury effect of EA on focal cerebral ischemia was limited. Above results suggest that the appropriate c-fos expression in brain may play a special role of brain protection on transient focal cerebral ischemia and EA may bring into a protective effect on brain ischemic infarction, via depressing part of superfluous brain c-fos expression, which may be one of the mechanisms of EA anti-injury in transient cerebral focal ischmia.