[Involvement of cerebral neuroglobin in electroacupuncture preconditioning-induced protection effect in cerebral ischemia-reperfusion rats]
- PMID: 23342777
[Involvement of cerebral neuroglobin in electroacupuncture preconditioning-induced protection effect in cerebral ischemia-reperfusion rats]
Abstract
Objective: To observe the effect of electroacupuncture (EA) preconditioning on cerebral ischemia and the role of cerebral neuroglobin (NgB) in EA-induced brain protection in focal cerebral ischemia and reperfusion injury (CI/RI) rats.
Methods: Male SD rats were randomly assigned to sham control, CI/RI 6 h, CI/RI 24 h and CI/RI 72 h groups (n = 6) for observing changes of NgB at different time-points. Additional SD rats were randomly assigned to sham, model, and EA preconditioning (EA-PC) groups (n = 16) for observing changes of cerebral NgB positive cell counts in the ischemic penumbra region 24 h after reperfusion. EA pre-conditioning was applied to "Baihui" (GV 20) for 30 min, once daily for 5 days before CI/RI. CI/RI model was established by occlusion of the right middle cerebral artery and reperfusion for 6 h, 24 h and 72 h respectively. The neurological behavior scores (NBS) of all the rats were evaluated according to Garcia's methods. The cerebral infarct volume was determined by 2,3,5-triphenyltetrazolium chloride (TTC) staining. The number of cerebral NgB positive cells was detected by immunofluorescent staining.
Results: No infarct loci were found in the sham group. The cerebral infarction volume percentage was significantly higher in the model group than in the EA-PC group (P < 0.01), while the NBS was significantly lower in the model group than in the EA-PC group (P < 0.01). The number of cerebral NgB positive cells in the ischemic penumbra was up-regulated 6 h after CI/RI injury, peaked at 24 h and continued at 72 h. Compared with the sham group, the number of cerebral NgB positive cells of the model group was increased significantly, whereas that of the EA-PC group up-regulated further obviously in comparison with the model group (P < 0.01).
Conclusion: EA pretreatment has a significant neuroprotective effect on cerebral ischemia-reperfusion, which is closely related to its effect in up-regulating NgB protein expression.
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