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Journal of Chinese Integrative Medicine ›› 2008, Vol. 6 ›› Issue (6): 632-637.doi: 10.3736/jcim20080617

• Original Experimental Research • Previous Articles     Next Articles

Electroacupuncture protects the brain against acute ischemic injury via up-regulation of delta-opioid receptor in rats

Xue-song Tian1, Fei Zhou1,2, Ru Yang1, Ying Xia2,3, Gen-chen Wu1, Jing-chun Guo1()   

  1. 1. National Key Laboratory of Medical Neurobiology, Department of Integrative Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, China
    2. Shanghai Research Center for Acumoxibustion and Meridians, Shanghai 201203, China
    3. School of Medicine, Yale University, New Heaven, CT 06515, United States of America
  • Received:2008-03-11 Online:2008-06-20 Published:2008-06-15
  • Contact: GUO Jing-chun E-mail:guojch@yahoo.com.cn

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Objective: To explore the effect of δ-opioid receptor (DOR) in electroacupuncture (EA) protecting the brain against acute ischemic injury.
Methods: Fifty-one rats were randomly divided into sham ischemia group, ischemia group, sham EA group, EA group, and EA+DOR antagonist (naltrindole) group. Transient focal cerebral ischemia (1 hour) was induced in rat brain by middle cerebral artery occlusion (MCAO) method. EA was applied on Shuigou (GV 26) and Neiguan (PC 6) for 30 min, starting immediately after the onset of reperfusion. Neurological deficit scores and volume of cerebral infarction were detected after 24-hour reperfusion. Other 12 rats were randomly divided into sham ischemia group, ischemia group, EA group and EA+naltrindole group. DOR protein expressions were assessed by Western blotting after 24-hour reperfusion.
Results: In comparison with the ischemia group and sham EA group, EA significantly reduced ischemic infarction and neurological deficits (P<0.05); EA significantly increased the expression of 60 kD DOR protein (P<0.05) and tended to increase that of 36 kD DOR protein (P>0.05). When naltrindole was combined with EA, the naltrindole completely abolished the EA-induced protection in ischemic infarction and neurological deficits, and also arrested the expression of DOR.
Conclusion: EA can up-regulate DOR expression and protect the brain from ischemia-reperfusion injury.

Key words: electroacupuncture, ischemic attack, transient, opioid receptor delta, rats

CLC Number: 

  • R245.31

Figure 1

Temporal changes in regional cerebral blood flow (rCBF) in the ischemic brain"

Figure 2

Cerebral infarct size in different groups after 24-hour ischemic infarction-reperfusion The infarct volume was assessed after 24-hour reperfusion following 1 h MCAO. The coronal sections of the rat brains in sham ischemia group (A), sham EA group (B), ischemis group (C), EA group (D) and naltrindole+EA group (E) were stained by cresyl violet. Note that EA reduced the infarction and naltrindole reversed the EA effect (F). △P<0.05, vs ischemia group; ▲P<0.05, vs naltrindole+EA group (one-way ANOVA)."

Figure 3

Neurological deficit scores of rats in different groups after 24-hour ischemic infarction-reperfusion The scores of neurological deficits were evaluated after 24-hour reperfusion. Note that EA significantly attenuated neurological deficits, which could be blocked by naltrindole. △P<0.05, vs ischemia group; ▲P<0.05, vs naltrindole+EA group (one-way ANOVA)."

Figure 4

DOR protein expression in brain tissues of rats in different groups after 24-hour ischemic infarction-reperfusion A shows representative blots of three signal bands of 60, 48 and 36 kD DOR proteins detected by rabbit polyclonal N-terminus-directed DOR antiserum. Actin is used as an internal standard. B, C and D depict the effects of sham ischemia, ischemia, ischemia+naltrindole+EA and ischemia+EA on DOR protein expression in the striatum after 24-hour reperfusion (B: 36 kD protein; C: 48 kD protein; D: 60 kD protein). Note that EA significantly increases the 60 kD protein and naltrindole abolishes this effect. *P<0.05, vs sham ischemia group; △P<0.05, vs ischemia group; ▲P<0.05, vsnaltrindole+EA group (one-way ANOVA)."

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