Objective: To observe effects of Yishen Huazhuo recipe (YSHZR) on the synaptic morphology and the expression of Ca2+ related kinase

calmodulin kinase Ⅱ (CaMKⅡ) and protein kinase C (PKC)

in the hippocampus of Alzheimer's disease (AD) rat

and explore the mechanism of YSHZR on the treatment of AD. Method: Fifty male SD rats were randomly divided into the sham group

model group

low

middle and high dose group of YSHZR. The β-amyloid fragment 25-35 (Aβ25-35) was injected into the left lateral ventricle of rats to establish AD rat model. Each dose group was treated by oral administration with 2.8

5.6

11.2 g · kg-1 of YSHZR

sham group and model group were given an equal volume of normal saline

and gavaged once daily for 4 weeks. The morphological changes of synapses in the rat hippocampus were observed by an electron microscope

and Western blot was used to measure the expression of CaMK Ⅱ and PKC in the rat hippocampus. Result: Compared with the sham group

the synaptic cleft in the hippocampus of model group rats was in fusion and blurred

presynaptic components were in severe edema

synaptic vesicles were severe reduced

the size was uneven

the vast majority of mitochondrial membrane and crest was in fusion

blurred and even disappeared. The crest mitochondrial was fractured and had cavitation. However

the three doses of YSHZR improved synaptic morphology to some extent

especially the low-dose group. In addition

compared with the model group

the number of synapses

gap of which was clear

was significantly increased (P<0.05) in low dose group of YSHZR;the number of synapses

gap of which showed partly fusion

had no significant change in each dose group of YSHZR;but the number of synapses

gap of whichshowed fully fusion

was significantly reduced (P<0.05). Western blot assay found that

compared with the sham group

the expression of CaMK Ⅱ and PKC in the rat hippocampus of model group was significantly decreased (P<0.05)

three dosages of YSHZR could significantly up-regulate the expression of CaMK Ⅱ and PKC (P<0.05). Conclusion: YSHZR may treat AD through improving the synapses morphology and promoting the expression of CaMKⅡand PKC in the hippocampus.