Objective To observe the effects of electroacupuncture(EA) on the expression levels of N-methyl-D-aspartate receptor(NMDAR)

extracellular signal-regulated kinase(ERK)1/2

p38 mitogen activated protein kinase(p38 MAPK) and c-Jun N-terminal kinase(JNK) in the spinal cord of rats with primary dysmenoramia(PDM)

so as to explore the underlying mechanism of EA treating PDM. Methods Thirty female SD rats were randomly divided into normal group

model group and EA group

with 10 rats in each group. The PDM rat model was established by subcutaneous injection of estradiol benzoate and oxytocin into the thigh. At the same time of modeling

rats in the EA group were treated with EA(50 Hz) at “Sanyinjiao”(SP36) and “Guanyuan”(CV4) once daily

20 min each time

for 10 consecutive days. The writhing times

writhing score and writhing latency were observed within 30 min after oxytocin injection. The uterine pathological morphology was observed by HE staining

and pathological score was calculated. Serum prostaglandin F2α(PGF2α) and prostaglandin E2(PGE2) were determined by ELISA. The protein expression levels of NMDAR

ERK1/2

p38MAPK and JNK in spinal cord were detected by Western blot. Results Compared with the normal group

the writhing times and writhing score were significantly increased(P<0.05); the endometrial epithelial cells showed vacuolar degeneration

death and hyperemia

the uterine pathological score was increased(P<0.05); the content of serum PGF2α and the ratio of PGF2α/PGE2 were significantly increased(P<0.01)

while the content of serum PGE2 was significantly decreased(P<0.01); the expression levels of NMDAR

ERK1/2

p38MAPK and JNK in spinal cord were significantly increased(P<0.05

P<0.01) in the model group. Compared with the model group

the writhing times and writhing score were significantly decreased(P<0.05)

the writhing latency was prolonged(P<0.05); the endometrial epithelial cells still showed vacuolar degeneration

death and hyperemia

and the uterine pathological score was decreased(P<0.01); the content of serum PGF2α and the ratio of PGF2α/PGE2 were significantly decreased(P<0.01)

while the content of serum PGE2 was significantly increased(P<0.01); the protein expression levels of ERK1/2 and JNK in spinal cord were significantly decreased(P<0.01) in the EA group. Conclusion EA intervention at SP36 and GV4 has obvious analgesic effect on PDM rats

and its mechanisms may be related to reducing serum prostaglandin

alleviating uterine inflammation

and inhibiting the protein expressions of NMDAR

ERK1/2

p38 MAPK and JNK in spinal cord.