摘要
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 。
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.
出处
《针刺研究》
CAS
CSCD
2001年第2期97-101,共5页
Acupuncture Research
基金
国家自然科学基金重点课题资助 (No.39735 10 )
