Effects of electroacupuncture on uterine prostaglandin F2α, cyclooxygenase 2 and nuclear factor κB in rats with primary dysmenorrhea / 针灸推拿医学（英文版）

ABSTRACT

Objective: To observe the effects of electroacupuncture (EA) on uterine prostaglandin F2α (PGF2α), cyclooxygenase 2 (COX-2) and nuclear factor κB (NF-κB) in rats with primary dysmenorrhea (PD) and to discuss the possible mechanism in EA intervening PD. Methods: Forty Sprague-Dawley female rats were randomly divided into a blank group, a model group, an EA group and an ibuprofen group, with 10 rats in each group. The PD model was established using estradiol benzoate combined with oxytocin in the model group, EA group and ibuprofen group. At the same time of modeling, rats in the EA group were given EA at Guanyuan (CV 4) and Sanyinjiao (SP 6) once a day for 20 min each time for 10 consecutive days. Ibuprofen was intragastrically administered once a day for 10 consecutive days in the ibuprofen group. The same amount of normal saline was intragastrically administered once a day for 10 consecutive days in the blank group and model group. The number of writhing of rats in each group within 30 min was compared on the 11th day just after the interventions. The uterine homogenate supernatant was separated and the PGF2α level was detected by enzyme-linked immunosorbent assay. Western blot was applied for the detection of the expression levels of COX-2, phospho-NF-κB p65 and NF-κB p65 proteins in uterine tissues. Results: Compared with the blank group, the number of writhing in the model group increased significantly (P<0.01), and the expression levels of PGF2α, COX-2, phospho-NF-κB p65 and NF-κB p65 proteins in uterine tissues were significantly increased (all P<0.01). Compared with the model group, the number of writhing in the EA group and ibuprofen group were significantly reduced (both P<0.01), and the expression levels of PGF2α and COX-2 protein in uterine tissues were significantly reduced (both P<0.01). Compared with the model group, the phospho-NF-κB p65 level in uterine tissues in the EA group was significantly reduced (P<0.01). Compared with the ibuprofen group, the phospho-NF-κB p65 level in the EA group was significantly reduced (P<0.01). Conclusion: The mechanism of EA for PD rats may be related to inhibiting the phosphorylation of NF-κB and reducing the levels of COX-2 and PGF2α in uterine tissues.