本研究旨在探讨葛根汤对原发性痛经(PD)小鼠模型下丘脑-垂体-卵巢轴(HPOA)功能障碍的调节作用。通过给予苯甲酸雌二醇和催产素建立具有周期性特征的PD小鼠模型。将小鼠随机分为对照组,模型,GGD,和布洛芬组。扭动的反应,下丘脑指数,垂体指数,卵巢指数,观察并测定子宫指数。前列腺素F_(2α)(PGF_(2α))、促性腺激素释放激素(GnRH),卵泡刺激素(FSH),黄体生成素(LH),用ELISA试剂盒测定雌激素(E_2)水平。蛋白质印迹和qPCR用于确定蛋白质和mRNA水平,分别,垂体组织中的促性腺激素释放激素受体(GnRH-R),卵巢组织中的促卵泡激素受体(FSHR)和促黄体生成素受体(LHR),和子宫组织中的雌激素受体(ER)。结果表明,扭动反应,血清PGF_(2α)水平,GnRH,FSH,LH,和E_2,卵巢和子宫指数,垂体组织中GnRH-R的蛋白质和mRNA水平,卵巢组织中的FSHR和LHR,与对照组相比,模型组子宫组织中的ER明显升高。GGD抑制了扭动反应,降低血清PGF_(2α)水平,GnRH,FSH,LH,和E_2,降低卵巢和子宫指数,并下调垂体组织中GnRH-R的蛋白和mRNA水平,卵巢组织中的FSHR和LHR,和子宫组织中的ER。数据表明,GGD可以通过下调与HPOA轴相关的蛋白质和基因的表达来调节HPOA并抑制复发性PD小鼠的E_2生成。从而发挥对PD的治疗作用。
This study aimed to explore the regulating effect of Gegen Decoction(GGD) on the hypothalamic-pituitary-ovarian axis(HPOA) dysfunction in the mouse model of primary dysmenorrhea(PD). The mouse model of PD with periodic characteristics was established by administration of estradiol benzoate and oxytocin. Mice were randomized into control, model, GGD, and ibuprofen groups. The writhing response, hypothalamus index, pituitary index, ovary index, and uterus index were observed and determined. The serum levels of prostaglandin F_(2α)(PGF_(2α)), gonadotropin-releasing hormone(GnRH), follicle-stimulating hormone(FSH), luteinizing hormone(LH), and estrogen(E_2) levels were measured by ELISA kits. Western blot and qPCR were employed to determine the protein and mRNA levels, respectively, of gonadotropin-releasing hormone receptor(GnRH-R) in the pituitary tissue, follicle-stimulating hormone receptor(FSHR) and luteinizing hormone receptor(LHR) in the ovarian tissue, and estrogen receptor(ER) in the uterine tissue. The results showed that the writhing response, serum levels of PGF_(2α), GnRH, FSH, LH, and E_2, ovarian and uterine indexes, the protein and mRNA levels of GnRH-R in the pituitary tissue, FSHR and LHR in the ovarian tissue, and ER in the uterine tissue were significantly increased in the model group compared with those in the control group. GGD inhibited the writhing response, reduced the serum levels of PGF_(2α), GnRH, FSH, LH, and E_2, decreased the ovarian and uterine indexes, and down-regulated the protein and mRNA levels of GnRH-R in the pituitary tissue, FSHR and LHR in the ovarian tissue, and ER in the uterine tissue. The data suggested that GGD can regulate the HPOA and inhibit E_2 generation in the mice experiencing recurrent PD by down-regulating the expression of proteins and genes related to HPOA axis, thus exerting the therapeutic effect on PD.