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Electroacupuncture Ameliorates Learning and Memory via Activation of the CREB Signaling Pathway in the Hippocampus to Attenuate Apoptosis after Cerebral Hypoperfusion.

Han X, Zhao X, Lu M, Liu F, Guo F, Zhang J, Huang X - Evid Based Complement Alternat Med (2013)

Bottom Line: Studies have shown that electroacupuncture (EA) ameliorates learning and memory after ischemic injury.In this study, we explored the cAMP response element-binding protein (CREB) signaling pathway-mediated antiapoptotic action involved in EA-induced improvement of learning and memory.Our findings indicated that (1) EA ameliorated spatial learning and memory impairment in cerebral hypoperfusion rats; (2) EA increased the immunoreactivities of pCREB and Bcl-2 and decreased the immunoreactivity of Bax; (3) intracerebroventricular administration of H89 (the inhibitor of protein kinase A) blocked EA-induced, pCREB-mediated antiapoptotic action and improved learning and memory.

View Article: PubMed Central - PubMed

Affiliation: Department of Rehabilitation Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

ABSTRACT
Studies have shown that electroacupuncture (EA) ameliorates learning and memory after ischemic injury. However, there have been few studies elucidating the mechanisms of EA on learning and memory in cerebral hypoperfusion. In this study, we explored the cAMP response element-binding protein (CREB) signaling pathway-mediated antiapoptotic action involved in EA-induced improvement of learning and memory. EA at GV20 and GV14 acupoints was applied in cerebral hypoperfusion rats. A Morris water maze task was performed, and the immunoreactivities of pCREB, Bcl-2, and Bax in the hippocampal CA1 area were evaluated by the Western blotting technique. Our findings indicated that (1) EA ameliorated spatial learning and memory impairment in cerebral hypoperfusion rats; (2) EA increased the immunoreactivities of pCREB and Bcl-2 and decreased the immunoreactivity of Bax; (3) intracerebroventricular administration of H89 (the inhibitor of protein kinase A) blocked EA-induced, pCREB-mediated antiapoptotic action and improved learning and memory. These results suggest that EA can ameliorate learning and memory via activation of the CREB signaling pathway in the hippocampus to attenuate apoptosis after cerebral hypoperfusion.

No MeSH data available.


Related in: MedlinePlus

Western blotting showing immunoreactivity of apoptosis-related proteins in the hippocampal CA1 area. The Bcl-2 and Bax protein values were calculated as a ratio of Bcl-2 and Bax protein to GAPDH. EA increased the expression of Bcl-2 and decreased the expression of Bax ((a) and (c)). However, the antiapoptotic action of EA was markedly inhibited by ICV injection of H89 ((b) and (d)). The data are expressed as the mean ± SEM. ANOVA statistical analyses were performed to compare the means among the control, model, and EA groups; △P < 0.01 compared with the control group; ▲P < 0.05 compared with the model group. A t-test was used to compare the means between the EA + NS and EA + H89 groups; *P < 0.05 compared with the EA + NS group.
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fig5: Western blotting showing immunoreactivity of apoptosis-related proteins in the hippocampal CA1 area. The Bcl-2 and Bax protein values were calculated as a ratio of Bcl-2 and Bax protein to GAPDH. EA increased the expression of Bcl-2 and decreased the expression of Bax ((a) and (c)). However, the antiapoptotic action of EA was markedly inhibited by ICV injection of H89 ((b) and (d)). The data are expressed as the mean ± SEM. ANOVA statistical analyses were performed to compare the means among the control, model, and EA groups; △P < 0.01 compared with the control group; ▲P < 0.05 compared with the model group. A t-test was used to compare the means between the EA + NS and EA + H89 groups; *P < 0.05 compared with the EA + NS group.

Mentions: One of the main mechanisms involved in the induction of the apoptotic pathway is the decrease in Bcl-2 levels or, alternatively, an increase in Bax levels. The Bcl-2 family is involved in cell death processes and plays a pivotal role in the cellular apoptotic machinery [24]. Bcl-2 is an antiapoptotic protein, and Bax exhibits proapoptotic activity [24, 25]. To investigate whether EA could attenuate apoptosis in the hippocampus after cerebral hypoperfusion, the immunoreactivities of Bcl-2 and Bax in the hippocampal CA1 area were examined by Western blotting analysis. Cerebral hypoperfusion had an effect on apoptosis in the hippocampal CA1 area as demonstrated by the decreased immunoreactivity of Bcl-2 and increased immunoreactivity of Bax in the model group rats compared with that of the control group. In the EA group, the immunoreactivity of Bcl-2 significantly increased and the immunoreactivity of Bax significantly decreased compared with that of the model group (Figures 5(a) and 5(c)). However, in EA + H89 group, the immunoreactivity of Bcl-2 significantly decreased and the immunoreactivity of Bax significantly increased compared with that of the EA + NS group (Figures 5(b) and 5(d)).


Electroacupuncture Ameliorates Learning and Memory via Activation of the CREB Signaling Pathway in the Hippocampus to Attenuate Apoptosis after Cerebral Hypoperfusion.

Han X, Zhao X, Lu M, Liu F, Guo F, Zhang J, Huang X - Evid Based Complement Alternat Med (2013)

Western blotting showing immunoreactivity of apoptosis-related proteins in the hippocampal CA1 area. The Bcl-2 and Bax protein values were calculated as a ratio of Bcl-2 and Bax protein to GAPDH. EA increased the expression of Bcl-2 and decreased the expression of Bax ((a) and (c)). However, the antiapoptotic action of EA was markedly inhibited by ICV injection of H89 ((b) and (d)). The data are expressed as the mean ± SEM. ANOVA statistical analyses were performed to compare the means among the control, model, and EA groups; △P < 0.01 compared with the control group; ▲P < 0.05 compared with the model group. A t-test was used to compare the means between the EA + NS and EA + H89 groups; *P < 0.05 compared with the EA + NS group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3817932&req=5

fig5: Western blotting showing immunoreactivity of apoptosis-related proteins in the hippocampal CA1 area. The Bcl-2 and Bax protein values were calculated as a ratio of Bcl-2 and Bax protein to GAPDH. EA increased the expression of Bcl-2 and decreased the expression of Bax ((a) and (c)). However, the antiapoptotic action of EA was markedly inhibited by ICV injection of H89 ((b) and (d)). The data are expressed as the mean ± SEM. ANOVA statistical analyses were performed to compare the means among the control, model, and EA groups; △P < 0.01 compared with the control group; ▲P < 0.05 compared with the model group. A t-test was used to compare the means between the EA + NS and EA + H89 groups; *P < 0.05 compared with the EA + NS group.
Mentions: One of the main mechanisms involved in the induction of the apoptotic pathway is the decrease in Bcl-2 levels or, alternatively, an increase in Bax levels. The Bcl-2 family is involved in cell death processes and plays a pivotal role in the cellular apoptotic machinery [24]. Bcl-2 is an antiapoptotic protein, and Bax exhibits proapoptotic activity [24, 25]. To investigate whether EA could attenuate apoptosis in the hippocampus after cerebral hypoperfusion, the immunoreactivities of Bcl-2 and Bax in the hippocampal CA1 area were examined by Western blotting analysis. Cerebral hypoperfusion had an effect on apoptosis in the hippocampal CA1 area as demonstrated by the decreased immunoreactivity of Bcl-2 and increased immunoreactivity of Bax in the model group rats compared with that of the control group. In the EA group, the immunoreactivity of Bcl-2 significantly increased and the immunoreactivity of Bax significantly decreased compared with that of the model group (Figures 5(a) and 5(c)). However, in EA + H89 group, the immunoreactivity of Bcl-2 significantly decreased and the immunoreactivity of Bax significantly increased compared with that of the EA + NS group (Figures 5(b) and 5(d)).

Bottom Line: Studies have shown that electroacupuncture (EA) ameliorates learning and memory after ischemic injury.In this study, we explored the cAMP response element-binding protein (CREB) signaling pathway-mediated antiapoptotic action involved in EA-induced improvement of learning and memory.Our findings indicated that (1) EA ameliorated spatial learning and memory impairment in cerebral hypoperfusion rats; (2) EA increased the immunoreactivities of pCREB and Bcl-2 and decreased the immunoreactivity of Bax; (3) intracerebroventricular administration of H89 (the inhibitor of protein kinase A) blocked EA-induced, pCREB-mediated antiapoptotic action and improved learning and memory.

View Article: PubMed Central - PubMed

Affiliation: Department of Rehabilitation Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

ABSTRACT
Studies have shown that electroacupuncture (EA) ameliorates learning and memory after ischemic injury. However, there have been few studies elucidating the mechanisms of EA on learning and memory in cerebral hypoperfusion. In this study, we explored the cAMP response element-binding protein (CREB) signaling pathway-mediated antiapoptotic action involved in EA-induced improvement of learning and memory. EA at GV20 and GV14 acupoints was applied in cerebral hypoperfusion rats. A Morris water maze task was performed, and the immunoreactivities of pCREB, Bcl-2, and Bax in the hippocampal CA1 area were evaluated by the Western blotting technique. Our findings indicated that (1) EA ameliorated spatial learning and memory impairment in cerebral hypoperfusion rats; (2) EA increased the immunoreactivities of pCREB and Bcl-2 and decreased the immunoreactivity of Bax; (3) intracerebroventricular administration of H89 (the inhibitor of protein kinase A) blocked EA-induced, pCREB-mediated antiapoptotic action and improved learning and memory. These results suggest that EA can ameliorate learning and memory via activation of the CREB signaling pathway in the hippocampus to attenuate apoptosis after cerebral hypoperfusion.

No MeSH data available.


Related in: MedlinePlus