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 receptorγcoactivator(PGC-1α)of hippocampal CA 1 region in Alzheimer's disease(AD)rats

so as to explore its mechanism underlying 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(n=10 in each).The AD model was established by intraperitoneal injection of D-Galactose(120 mg·kg

(-1)

·d(-1)·d

(-1)

)combined with bilateral hippocampal injection ofβamyloid 1-40(Aβ1-40).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 Gastrodin 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-1αof hippocampal CA 1 region was measured by immunohistochemical staining.Results 1)Morris water maze tests showed that

compared with the normal and sham group

the escape latency was significantly prolonged(P

<

0.05)

and the percentage of platform quadrant residence duration and the platform crossing times were considerably decreased in the model group(P

<

0.05).After the intervention

the escape latency was obviously shortened(P

<

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(P

<

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 the3 treatment groups than in the model group.3)The expression levels of SIRT 1 and PGC-1αproteins in the hippocampal CA 1 area were significantly down-regulated in the model group than in the normal and sham groups(P

<

0.05).After the intervention

the expression levels of SIRT 1 and PGC-1αin the EA

Gastrodin and EA+Gastrodin groups were significantly up-regulated compared with the model group(P

<

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-1αas well as in increasing the percentage of platform quadrant residence time and platform crossing times(P

<

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-1αand reducing neuronal injury in the CA 1 region of hippocampus

suggesting aprotective role of EA on hippocampal neurons.The effect of EA combined with Gastrodin is markedly better than that of EA and Gastrodin alone.