| Objective: To investigate whether electroacupuncture (EA) protects hippocampal neurons from apoptosis and its probable mechanism in rats following cerebral hypoperfusion. Methods: Ninety male Sprague-Dawley (SD) rats were randomly divided into five groups: a sham-operated control group (Con), a model group (Mod), an EA group (EA), an EA combined with intracerebroventricular (ICV) injection of PKA blocker H89 group (EA+H89) and an EA combined with ICV injection of normal saline (NS) group (EA+NS). Each group included three time courses: 7 days, 14 days and 21 days. Cerebral hypoperfusion was induced by permanent and bilateral common carotid artery occlusion (2-vessel occlusion, 2VO). EA was given on GV20 and GV14. TUNEL and Western blotting were employed to observe apoptosis of neurons and expression changes of Bax and Bcl-2 proteins of the hippocampus. Results: In the Mod group, the apoptosis rate was significantly higher on day 14 and 21 than on day 7 (P<0.05), and there was no significant difference in other groups among the three time points. In the EA group, the expression of Bcl-2 protein was significantly higher in the 21-day subgroup than in the 14-day subgroup (P<0.05), and there were no significant differences in other groups. Percentages of apoptotic neurons were higher in the Mod group than in the Con group (P<0.05), but lower in the EA group than in the Mod group (P<0.05). In the EA+H89 group, protecting effects of EA were weakened, and those in the EA+NS group had no significant change. Western blotting suggested that the expression of Bax protein was significantly up-regulated (P<0.05) and that of Bcl-2 protein significantly down-regulated (P<0.05) in the Mod group as compared with the Con groups, and the Bax protein significantly reduced (P<0.05) and the Bcl-2 protein significantly increased (P<0.05) in the EA group as compared with the Mod group. In the EA+H89 group, the Bax protein was significantly increased (P<0.05) and the Bcl-2 protein significantly decreased (P<0.05) as compared with the EA+NS group (the expression of Bcl-2 protein had no significant difference on the day 14). Conclusion: EA on GV20 and GV14 could alleviate apoptosis of hippocampal neurons by regulating the expression of Bax and Bcl-2 proteins after cerebral hypoperfusion, and the above effects could be inhibited by PKA blocker H89, suggesting that EA might exert antiapoptotic effects through activation of the PKA-CREB signaling pathway. |
