■原发性痛经(PD)的现有治疗方法,如NSAIDs,赋予副作用。葛根汤(GGD),中药,在治疗PD方面表现出了希望,但其确切机制尚不清楚。这里,我们旨在使用大鼠模型研究GGD缓解PD的效率,以了解其确切的作用机制。
■我们建立了雌二醇和催产素诱导的大鼠痛经模型。PD大鼠每天一次胃内给药GGD或布洛芬(阳性对照),连续七天。血清前列腺素E2(PGE2)水平,前列腺素F2α(PGF2α),β-内啡肽(β-EP),血栓烷B2(TXB2),使用酶联免疫吸附测定(ELISA)测定6-酮-前列腺素F1α(6-酮-PGF1α)。采用免疫组织化学方法检测子宫组织中雌激素受体α(ERα)和环氧合酶-2(COX-2)的表达水平,磷酸化和总细胞外信号调节蛋白激酶1和2(ERK1/2)的那些使用蛋白质印迹分析进行评估。
■用GGD处理显著减少扭体行为,组织病理学评分,以及PD大鼠血清中COX-2、PGE2和PGF2α的水平。此外,GGD增加子宫组织中β-EP含量,抑制ERK1/2活化和ERα表达。
■这项研究的结果表明,GGD通过抑制COX-2介导的PGE2和PGF2α的释放来减轻大鼠的PD,调节ERα/ERK1/2/COX-2通路,增加β-EP含量。这些结果提供了对GGD治疗PD的潜在机制的见解,并支持其作为这种疾病的替代疗法的进一步研究。
葛根汤常用于缓解原发性痛经。然而,其抗痛经的机制仍然难以捉摸。在这项研究中,使用原发性痛经的大鼠模型,我们证明Ge-Gen汤降低了血清中环氧合酶-2,前列腺素E2和前列腺素F2α的水平,并使子宫中的细胞外信号调节蛋白激酶1和2磷酸化。这些结果表明,Ge-Gen汤通过使雌激素受体α/细胞外信号调节蛋白激酶1和2/环氧合酶-2途径失活来减轻原发性痛经。这项研究增强了我们对原发性痛经发病机理的理解,并可能为新型治疗方法的发展提供潜在的信息。
UNASSIGNED: Existing treatments for primary dysmenorrhoea (PD), such as NSAIDs, impart side effects. Ge-Gen decoction (GGD), a traditional Chinese medicine, has shown promise in treating PD, but its exact mechanisms remain unclear. Here, we aimed to investigate the efficiency of GGD in alleviating PD using a rat model to understand its precise mechanism of action.
UNASSIGNED: We established a rat model of dysmenorrhoea induced by oestradiol and oxytocin. The PD rats were administered GGD or Ibuprofen (positive control) intragastrically once daily for seven consecutive days. Serum levels of prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2α), β-endorphin (β-EP), thromboxane B2 (TXB2), 6-keto-prostaglandin F1α (6-keto-PGF1α) were determined using an enzyme-linked immunosorbent assay (ELISA). The expression levels of oestrogen receptor alpha (ERα) and cyclooxygenase-2 (COX-2) in uterine tissue were measured using immunohistochemical assays, and those of phosphorylated and total extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) were assessed using western blot analysis.
UNASSIGNED: Treatment with GGD significantly reduced writhing behaviour, histopathological scores, and levels of COX-2, PGE2, and PGF2α in the serum of PD rats. Additionally, GGD increased β-EP content and inhibited ERK1/2 activation and ERα expression in uterine tissues.
UNASSIGNED: The results of this study suggest that GGD alleviates PD in rats by suppressing the COX-2-mediated release of PGE2 and PGF2α, modulating the ERα/ERK1/2/COX-2 pathway, and increasing β-EP content. These results provide insights into the potential mechanisms of GGD in treating PD and support its further investigation as an alternative therapy for this condition.
Ge-Gen decoction is commonly used to alleviate primary dysmenorrhoea. However, its anti-dysmenorrhoea mechanism remains elusive. In this study, using a rat model of primary dysmenorrhoea, we demonstrate that Ge-Gen decoction reduced the levels of cyclooxygenase-2, prostaglandin E2, and prostaglandin F2 alpha in serum and phosphorylated extracellular signal-regulated protein kinases 1 and 2 in the uterus. These results suggest that Ge-Gen decoction alleviates primary dysmenorrhoea via inactivation of the oestrogen receptor alpha/extracellular signal-regulated protein kinases 1 and 2/cyclooxygenase-2 pathway. This study enhances our understanding of the pathogenesis of primary dysmenorrhoea and may potentially inform the development of novel treatment approaches.