Effects of electroacupuncture on uterine prostaglandin F_2α, cyclooxygenase 2 and nuclear factor κB in rats with primary dysmenorrhea

Abstract

Objective

To observe the effects of electroacupuncture (EA) on uterine prostaglandin F_2α (PGF_2α), 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 PGF_2α 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 PGF_2α, 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 PGF_2α 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 PGF_2α in uterine tissues.

摘要

目的:观察电针对原发性痛经(PD)大鼠子宫组织前列腺素F_2α(PGF_2α)、环氧化酶2(COX-2)和核因子κB (NF-κB) 的影响, 探讨电针干预PD的可能机制。方法:将40只Sprague-Dawley雌性大鼠随机分为正常组、模型组、电针组 和布洛芬组, 每组10只。模型组、电针组和布洛芬组采用苯甲酸雌二醇联合缩宫素建立PD大鼠模型。造模同时, 电 针组大鼠给予电针关元和三阴交治疗, 每日1次, 每次20 min, 连续10 d; 布洛芬组给予布洛芬灌胃干预, 每日1次, 连续10 d; 正常组和模型组给予等量的生理盐水灌胃, 每日1次, 连续10 d。于第11天比较各组大鼠30 min内扭体 次数; 酶联免疫吸附测定法检测子宫匀浆上清液中PGF_2α水平; Western blot检测子宫组织COX-2、磷酸化NF-κB p65 (phospho-NF-κB p65)及NF-κB p65的蛋白表达水平。结果:与正常组相比, 模型组大鼠扭体次数明显增多(P<0.01), 子宫组织PGF_2α含量、COX-2、phospho-NF-κB p65及NF-κB p65蛋白水平明显升高(均P<0.01)。与模型组相比, 电针 组和布洛芬组扭体次数明显减少(均P<0.01), 子宫组织PGF_2α含量和COX-2蛋白水平明显降低(均P<0.01)。与模型 组相比, 电针组大鼠子宫组织phospho-NF-κB p65蛋白水平明显降低(P<0.01)。与布洛芬组相比, 电针组大鼠子宫 组织phospho-NF-κB p65蛋白水平明显降低(P<0.01)。结论:电针干预PD大鼠的作用机制可能与抑制子宫组织中 NF-κB磷酸化, 降低子宫组织COX-2和PGF_2α水平有关。