Objective To observe the effect of electroacupuncture(EA) on learning-memory ability

ultrastructural changes of hippocampal CA1 neurons

reactive oxygen species(ROS) level

Nod-like receptor protein 3(NLRP3) and auto-phagy-related proteins expression in the hippocampus of vascular dementia(VD) rats

so as to reveal its partial mechanisms in treating VD. Methods Male SD rats were randomly divided into sham operation

model

and EA groups(n=10 rats in each group). The VD model was established by permanent ligation of bilateral common carotid arteries. Rats of the EA group were treated with EA at “Baihui”(GV20)

“Dazhui”(GV14) and bilateral “Shenshu”(BL23) for 30 min

once a day for 4 weeks. Morris water maze was used to evaluate the learning and memory ability of rats before modeling

4 weeks after modeling and after intervention. Transmission electron microscopy(TEM) was used to observe the ultrastructural changes of hippocampal CA1 neurons. The level of ROS in hippocampus was detected by DCFH-DA fluorescence probe. The expressions of NLRP3

autophagy-related protein Beclin1 and microtubule-associated protein 1 light chain 3(LC3) were measured by Western blot. Results In comparison with the sham operation group

the average escape latency of rats in the model group was prolonged(P<0.01)

and the times of crossing the original platform were reduced(P<0.05)

the level of ROS

the expression levels of LC3-Ⅱ/LC3-Ⅰ ratio

Beclin1 and NLRP3 proteins in hippocampus were increased(P<0.01

P<0.05) in the model group. After EA intervention

the average escape latency of rats was significantly shortened(P<0.01)

and the times of crossing the original platform were increased(P<0.05)

the level of ROS

the expression levels of LC3-Ⅱ/LC3-Ⅰ ratio

Beclin1 and NLRP3 proteins in hippocampus were decreased(P<0.01

P<0.05) in the EA group compared with those of the model group. Outcomes of TEM showed that CA1 neurons in the hippocampus were damaged

chromatin aggregation

mitochondria pyknosis

cristae structure disorder

rough endoplasmic reticulum expanded and degranulated

the number of free ribosomes decreased

and autophagy could be seen in the model group

which were milder in the EA group. Conclusion EA at GV20

GV14 and BL23 can improve the learning and memory abilities of VD rats

alleviate the ultrastructural damage of neurons in hippocampal CA1 area

and repair the damaged neurons. The mechanism may be related to the reduction of ROS level

LC3-Ⅱ/LC3-Ⅰ ratio

NLRP3 and Beclin1 protein expression

the decrease of neuronal autophagy

inhibition of activation of NLRP3 inflammasome and alleviation of central inflammatory response.