Background Transmembrane and intracellular signal transduction of G protein is closely related to the pathophysiology of Alzheimer's disease (AD).
Objective To explore the effects of Sanjiao acupuncture on G protein signal transduction pathways in the pathogenesis of AD.
Methods 36 senescence-accelerated (SAM) prone 8 mice were divided into three groups that remained untreated (SAMP8, n=12) or received Sanjiao acupuncture (SAMP8+SA, n=12) or control acupuncture (SAMP8+CA, n=12). An additional control group of SAM resistant 1 mice was included (SAMR1 group, n=12). Morris water maze tests were used to investigate learning and memory abilities. Immunoprecipitation and Western blotting were used to study expression of G protein subunits and their activities in the cortex/hippocampus.
Results Behavioural analysis showed that acupuncture attenuated the severe cognitive deficits observed in untreated/CA-treated SAMP8 mice. The findings of the G protein activation assays via immunoprecipitation and Western blots were that the physiologically coupled activation rate (PCAR) and maximal coupled activation rate (MCAR) of Gαs and Gαi were decreased in the cortex of SAMP8 vs SAMR1 mice. Sanjiao acupuncture induced an upregulation in the PCAR of Gαs and Gαi. In the hippocampus of untreated SAMP8 mice, the PCAR of Gαs and MCAR of both Gαs and Gαi declined, and Sanjiao acupuncture was associated with an upregulation in the MCAR of Gαs and Gαi. There were no significant differences in Gαs and Gαi expression between the groups.
Conclusions Sanjiao acupuncture attenuates cognitive deficits in a mouse model of AD via upregulation of G protein activity and stabilisation of the cellular signal.
- COMPLEMENTARY MEDICINE
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BL and LZ contributed equally.
Contributors JY conceived the study. BL and LZ drafted the paper. XZ, BK and YL conducted the animal experiments and collected the data. YJ and JH analysed the results and revised the paper. All authors approved the final version accepted for publication.
Funding This work was supported by the National Natural Science Foundation of China (grant no. 81202740 and 81273937), Specialised Research Fund for the Doctoral Program of Higher Education (grant no. 20121210110010 and 20121210120002) and Tianjin Natural Science Fund (grant no. 12JCQNJC07400).
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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