Objective: To investigate the protective effect of electroacupuncture (EA) on injured neurons and the signal transduction mechanism of calmodulin (CaM) in rats with cerebral ischemia-reperfusion injury (CIRI).
Methods: A total of 25 SD rats were randomly divided into a sham-operation group, a model group, an EA. group, a TFP group and an EA+TFP group. The rat model of middle cerebral artery occlusion (MCAO) was established by the modified Longa thread occlusion method. The EA group was treated with EA at "Dazhui" (GV 14) and "Baihui" (GV 20) for 30 minutes. The TFP group was treated with lumbar intrathecal injection of Trinuoperazine (TFP) at a dose of 40 microL/kg, the inhibitor of CaM. The EA + TFP group was treated with EA combined with TFP, and the sham-operation group and the model group without any treatment. The neurology deficit score was evaluated by the Julio's neuroethology score methods in all rats, and the expression of CaM in cerebral hippocampus tissue was detected with immunohistochemical method in different intervention condition.
Results: (1) In comparison with the model group of 6.90 +/- 1.66, the neuroethology score in the EA group of 14.50 +/- 1.08, the TFP group of 11.70 +/- 1.06 and the EA + TFP group of 14.30 +/- 1.06 were all significantly increased (all P < 0.01), while those still were all lower than the sham group of 17.60 +/- 0.52 (all P < 0.01), and the EA group was better than the TFP group (P < 0.01). (2) In comparison with the sham group of 0.080 +/- 0.045, the immune positive expression score of CaM protein in hippocampus in the model group of 1.680 +/- 0.268 was sig nificantly increased (P < 0.01). In comparison with the model group, the expression score of CaM protein in the EA group of 0.880 +/- 0.179, the TFP group of 0.720 +/- 0.179 and the EA + TFP group of 0.420 +/- 0.249 were all significantly reduced (all P < 0.01), and the expression score of CaM in the EA + TFP group was lower than that in the TFP group (P < 0.05).
Conclusion: EA can reduce the injury of cerebral neurons induced by CIRI in rats and promote the recovery, which may be related to its effect in regulating CaM signaling pathway after the ischemia-reperfusion injury.
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