Objective To observe the effect of electroacupuncture(EA) on the cognitive impairment and expressions of inositol-dependent kinase 1α(IRE1α)/c-Jun N-terminal kinase(JNK) pathway-related proteins in diabetic mice

so as to explore its underlying mechanism. Methods Thirty db/db mice were randomly divided into model group(n=15) and EA group(n=15)

and 15 db/m mice were chosen as the control group. EA was applied to “Baihui”(GV20) and “Shenting”(GV24)

bilateral “Pishu”(BL20) and “Shenshu”(BL23)

“Zusanli”(ST36) and “Sanyinjiao”(SP6) for 20 min

and bilateral “Feishu”(BL13)

“Hegu”(LI4) and “Taichong”(LR3) were stimulated with filiform needles

with the needles retained for 20 min

once daily

6 days a week for 4 weeks. The daily food intake

water intake

and weekly body weight and blood glucose of the mice in each group were recorded. The learning and memory abilities were detected by Morris water maze

the morphology of hippocampal cells was observed by HE staining

and IRE1α-JNK pathway-related proteins IRE1α

JNK

anti-apoptotic protein(Bcl-2) were detected by Western blot. Results Compared with the control group

the food intake

water intake

body weight

blood glucose in the mo-del group were significantly increased(P<0.01)

the escape latency was significantly prolonged(P<0.05)

the times of cros-sing platform were significantly reduced(P<0.01)

and the expression levels of IRE1α and JNK proteins were significantly increased(P<0.01)

while the expression of Bcl-2 protein was significantly decreased(P<0.01). Compared with the model group

the food and water intake in the EA group were significantly decreased(P<0.01)

the body weight and blood glucose were significantly decreased(P<0.05

P<0.01)

the escape latency was significantly shortened(P<0.05)

the times of crossing platform significantly increased(P<0.05)

and the expression levels of IRE1α and JNK proteins were significantly decreased(P<0.05)

while the Bcl-2 expression was significantly increased(P<0.01). The cells in hippocampal CA1 area of mice in the model group are in disorder

with unclear nuclei and obvious vacuoles; while the morphology of nerve cells in EA group was significantly improved. Conclusion EA can improve the cognitive impairment of db/db mice

as well as regulate body weight

blood glucose

and improve the cell morphology in the hippocampus

which may be related to its function in regulating the IRE1α-JNK pathway and related proteins.