本文对即早表达基因c fos在电针抗局灶性脑缺血损伤中的作用进行了探讨。结果表明

局灶性脑缺血可以引起c fos在缺血侧皮层的大量表达

电针能部分抑制这种表达

使局灶性脑缺血动物模型的脑梗塞灶减小。但c fos反义寡核苷酸脑内注射可完全阻断c fos表达

导致脑梗塞灶体积明显增大 ;同时也取消了电针的抗脑缺血损伤作用。提示脑内c fos适度的表达

可能在脑缺血损伤中有一定的保护作用 ;电针可能通过部分抑制脑内c fos的过度表达

发挥其抗局灶性脑缺血损伤的作用Objective: To explore the role of c fos expression (one early gene) in electroacupuncture (EA) resisting cerebral focal ischemic injury in the rat. Methods: ① 36 SD rats were randomly divided into ischemia group and ischemia + EA group each of that was further divided into 6 subgroups according to the duration of reperfusion (1 hr

2 hr

4 hr

8 hr

12 hr and 24 hr) after 90 min of cerebral ischemia. “Baihui" (GV 20) and “Shuigou" (GV 26) were stimulated with EA (3.5 mA

100 Hz

60 min). ② 24 SD rats were randomly and evenly divided into antisense

sense

mismatch and normal saline (NS) groups. C fos antisense (3 nmol/2 μL)

sense (2 μL)

mismatch (2 μL) and NS(2 μL) were separately injected into the ischemic central area of the rat brain (APO

L: 3.5 mm

H: 5.5 mm) in different groups. ③ The brain samples were stained with immunohistochemical (ABC) method and c fos positive neurons were calculated under microscope. Results: ① From the first hour on after cerebral ischemia and reperfusion

heavy expression of c fos appeared in the cortex of the ischemic side

it peaked at 4 hr and lowered from 8 hr on. Till 24 hr after ischemia

c fos expression quantity was similar on the ischemia and non ischemia sides. In acupuncture+ischemia group

c fos positive neuron count was significantly less than that of ischemia group. ② After microinjection of antisense in antisense group

fewer c fos positive neurons were seen around the ischemic region; while more c fos positive neurons found in sense group

mismatch group and NS group. The percentages of infarction volume/whole brain volume in antisense

sense

mismatch and NS were 12.69±6.67

2.27±0.93

2.69±1.39 and 2.51±1.77 respectively

that of antisense group was significantly larger than those of the rest 3 groups (P<0.05). Conclusion: Appropriate expression of c fos may have a certain protective action on cerebral ischemic injury; the inhibitory effect of EA on the superfluous expression of c fos in the brain may contribute to its resisting ischemic injury effect on cerebral neurons.