Both electroacupuncture and Gastrodin can improve the learning-memory ability of Alzheimer's disease. - GreenMedInfo Summary
[Electroacupuncture plus Gastrodin Improves Learning-memory Ability Possibly by Up-regulating Expression of SIRT 1 and PGC-1ɑ in Hippocampal CA 1 Region of Alzheimer's Disease Rats].
Zhen Ci Yan Jiu. 2018 Mar 25 ;43(3):140-5. PMID: 29560628
Rui Huang
OBJECTIVE: To observe the effect of electroacupuncture (EA) combined with Gastrodin on learning-memory ability and expression of silent information regulator 2 homologous protein 1(SIRT 1) and peroxisome proliferator activated receptorγ coactivator (PGC-1 ɑ) of hippocampal CA 1 region in Alzheimer's disease(AD) rats, so as to explore its mechanism under-lying improvement of AD.
METHODS: Sixty male SD rats were randomly divided into normal control (normal), sham operation (sham), model, EA, Gastrodin and EA+ Gastrodin groups (=10 in each). The AD model was established by intraperitoneal injection of D-Galactose (120 mg•kg•d) combined with bilateral hippocampal injection ofβ amyloid 1-40(Aβ 1-40). EA was applied at"Baihui"(GV 20),"Dazhui"(GV 14) and"Zusanli"(ST 36) for 30 min, once daily for 4 weeks. For rats of the Gastro-din group and EA+ Gastrodin group, intraperitoneal injection of gastrodin(10 mg/kg) was conducted once daily for 4 weeks. Morris water maze tests were used to assess the rat's learning-memory ability. Nissl staining was used to assess the morphological changes of neurons in the hippocampal CA 1 area. The expression of SIRT 1 and PGC-1 ɑ of hippocampal CA 1 region was mea-sured by immunohistochemical staining.
RESULTS: 1) Morris water maze tests showed that, compared with the normal and sham group, the escape latency was significantly prolonged (<0.05), and the percentage of platform quadrant residence duration and the platform crossing times were considerably decreased in the model group (<0.05). After the intervention, the escape latency was obviously shortened (<0.05), and the percentage of platform quadrant residence duration and the platform crossing times were markedly increased in the EA, Gastrodin and EA+Gastrodin groups relevant to the model group (<0.05). 2) Nissl staining showed that, in comparison with the normal group or sham group, the number of cells in the hippocampal CA 1 area was decreased and the arrangement was disorganized in the model group. The number of cells in CA 1 area was relatively higher in the 3 treatment groups than in the model group. 3) The expression levels of SIRT 1 and PGC-1ɑ proteins in the hippocampal CA 1 area were significantly down-regulated in the model group than in the normal and sham groups (<0.05). After the intervention, the expression levels of SIRT 1 and PGC-1ɑ in the EA, Gastrodin and EA+Gastrodin groups were significantly up-regulated compared with the model group (<0.05). The effects of EA+Gastrodin were significantly superior to those of simple EA and simple Gastrodin in shortening the escape latency, up-regulating the expression levels of SIRT 1 and PGC-1 ɑ as well as in increasing the percentage of platform quadrant residence time and platform crossing times (<0.05).
CONCLUSION: Both EA and Gastrodin can improve the learning-memory ability of AD rats, which may be related to their effects in up-regulating the expression of SIRT 1 and PGC-1ɑ and reducing neuronal injury in the CA 1 region of hippocampus, suggesting a protective role of EA on hippocampal neurons. The effect of EA combined with Gastrodin is markedly better than that of EA and Gastrodin alone.