OBJECTIVE: To observe the effect of electroacupuncture (EA) intervention combined with medication (Gastrodin) on changes of neurological function and expression of Nogo-A and Nogo-A receptor (NgR) in the frontal lobe cortex around the ischemic loci of focal cerebral ischemia (FCI) rats, so as to explore its mechanism underlying improvement of neuroregeneration of FC. METHODS: Fifty male Sprague-Dawley rats were randomly divided into normal control, model, EA, medication and EA+ medication groups (n = 10 in each group). The FCI model was induced by occlusion of the middle cerebral artery (MCAO) with thread embolus. EA was applied to the left "Quchi" (LI 11) and "Hegu" (Li 4) for 30 min, once daily for 14 days after MCAO. For rats of the medication group, Gastrodin (10 mg/kg) was administrated by intraperitoneal injection, once daily for 14 days. The neurological impairment was assessed by Zea Longa's scoring. The expression of Nogo-A and NgR in the frontal lobe cortex around the ischemic loci was detected by immunohistochemistry. RESULTS: In comparison with the normal control group, cerebro- cortical Nogo-A and NgR expression levels of the model group vere significantly increased (P < 0.05). Compared with the model group, the Zea Longa's score and Nogo-A and NgR expression levels were evidently down-regulated in the EA, medication and EA + medication groups (P < 0.05). The Zea Longa's score and Nogo-A and NgR expression levels were significantly lower in the EA + medication group than in the EA and medication groups (P < 0.05). CONCLUSION: EA intervention and Gastrodin administration can down-regulate cerebro-cortical Nogo-A and NgR protein expression in FCI rats, which may contribute to their action in improving neurological impairment. The effect of EA+ Gastrodin is better than simple EA or Gastrodin treatment.
OBJECTIVE: To observe the effect of electroacupuncture (EA) intervention combined with medication (Gastrodin) on changes of neurological function and expression of Nogo-A and Nogo-A receptor (NgR) in the frontal lobe cortex around the ischemic loci of focal cerebral ischemia (FCI) rats, so as to explore its mechanism underlying improvement of neuroregeneration of FC. METHODS: Fifty male Sprague-Dawley rats were randomly divided into normal control, model, EA, medication and EA+ medication groups (n = 10 in each group). The FCI model was induced by occlusion of the middle cerebral artery (MCAO) with thread embolus. EA was applied to the left "Quchi" (LI 11) and "Hegu" (Li 4) for 30 min, once daily for 14 days after MCAO. For rats of the medication group, Gastrodin (10 mg/kg) was administrated by intraperitoneal injection, once daily for 14 days. The neurological impairment was assessed by Zea Longa's scoring. The expression of Nogo-A and NgR in the frontal lobe cortex around the ischemic loci was detected by immunohistochemistry. RESULTS: In comparison with the normal control group, cerebro- cortical Nogo-A and NgR expression levels of the model group vere significantly increased (P < 0.05). Compared with the model group, the Zea Longa's score and Nogo-A and NgR expression levels were evidently down-regulated in the EA, medication and EA + medication groups (P < 0.05). The Zea Longa's score and Nogo-A and NgR expression levels were significantly lower in the EA + medication group than in the EA and medication groups (P < 0.05). CONCLUSION: EA intervention and Gastrodin administration can down-regulate cerebro-cortical Nogo-A and NgR protein expression in FCIrats, which may contribute to their action in improving neurological impairment. The effect of EA+ Gastrodin is better than simple EA or Gastrodin treatment.