Evidence Details for App
PMID Title Journal Year Abstract
25810743 Electroacupuncture Suppressed Neuronal Apoptosis and Improved Cognitive Impairment in the AD Model Rats Possibly via Downregulation of Notch Signaling Pathway. Evid Based Complement Alternat Med. 2015;2015:393569. doi: 10.1155/2015/393569. Epub 2015 Feb 25. 2015 Acupuncture is a potential strategy for the treatment of Alzheimer's disease (AD) and the possible mechanisms worth to be explored. In this study, we proposed and tested the hypothesis that whether Notch signaling pathway is involved in the effect of electroacupuncture (EA) treatment. Rats that received EA treatment on the acupoints of Baihui (Du 20) and Shenshu (BL 23) had shorter latency and remained in the original platform quadrant longer and crossed the former platform contained quadrant more frequently compared to the Abeta injection rats without EA treatment. EA obviously alleviated the cell apoptosis resulted by Abeta infusion in hippocampus CA1 regions through upregulating the expression of Bcl-2 and downregulating the expression of Bax. EA could further obviously promote the expression of synapsin-1 and synaptophysin in hippocampus. Abeta injection significantly increased the expression of Notch1, Jag1, and Hes1 mRNA, while EA treatment downregulated the level of Notch1 and Hes1 mRNA in hippocampus, but not Jag1 mRNA. Our data suggested that EA treatment improved learning and memory function in the AD rat model partially through downregulating Notch signaling pathway."

Evidence Sentence: Rats that received EA treatment on the acupoints of Baihui (Du 20) and Shenshu (BL 23) had shorter latency and remained in the original platform quadrant longer and crossed the former platform contained quadrant more frequently compared to the Abeta injection rats without EA treatment.
Evidence Sentence: EA obviously alleviated the cell apoptosis resulted by Abeta infusion in hippocampus CA1 regions through upregulating the expression of Bcl-2 and downregulating the expression of Bax.
Evidence Sentence: Abeta injection significantly increased the expression of Notch1, Jag1, and Hes1 mRNA, while EA treatment downregulated the level of Notch1 and Hes1 mRNA in hippocampus, but not Jag1 mRNA.
Evidence Sentence: The effects of EA on learning and memory ability in Abeta 1-40 infused rats were assessed using Morris water maze test.
Evidence Sentence: The escape latencies in Abeta 1-40 injected rats were significantly higher than those in control group in each same day from days 2 (P < 0.05 and P < 0.01).
Evidence Sentence: EA Attenuated the Neuronal Apoptosis Induced by Abeta
Evidence Sentence: The results showed that the number of cells with condensed and fragmented DNA (apoptotic cells) significantly increased after Abeta injection compared to the control group (P < 0.01), while EA obviously alleviated the cell apoptosis resulted by Abeta infusion in hippocampus CA1 regions (P < 0.01).
Evidence Sentence: Samples from Abeta injected rats represented much lower level of Bcl-2 and higher level of Bax than in the control group (P < 0.01).
Evidence Sentence: These data indicated that EA could balance the expression of apoptosis related proteins Bcl-2 and Bax and prevent the neuronal apoptosis induced by Abeta in hippocampus.
Evidence Sentence: Data from both immunohistochemistry staining and Western blot showed that the level of synapsin-1 was markedly decreased owing to Abeta injection (P < 0.01).
Evidence Sentence: Similarly, the level of synaptophysin in Abeta injected rats was much higher than that in control group (P < 0.05) and EA effectively increased the expression of synaptophysin compared to both model and sham-EA groups (P < 0.05; Figures 3(b) and 3(c)).
Evidence Sentence: Abeta injection obviously stimulated the expression of Notch1, Jag1, and Hes1 mRNA (P < 0.05 and P < 0.01).