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水煎剂可缓解大鼠原发性痛经症状。

decoction alleviates primary dysmenorrhoea symptoms in a rat model.

机构信息

Department of Gynaecology, Taicang Traditional Chinese Medicine Hospital, Affiliated to Nanjing University of Chinese Medicine, Taicang, Jiangsu, China.

Department of Anorectal Surgery, Taicang Traditional Chinese Medicine Hospital, Affiliated to Nanjing University of Chinese Medicine, Taicang, Jiangsu, China.

出版信息

J Obstet Gynaecol. 2024 Dec;44(1):2337691. doi: 10.1080/01443615.2024.2337691. Epub 2024 Apr 9.

Abstract

BACKGROUND

Existing treatments for primary dysmenorrhoea (PD), such as NSAIDs, impart side effects. 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.

METHODS

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.

RESULTS

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.

CONCLUSIONS

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.

摘要

背景

现有的原发性痛经(PD)治疗方法,如 NSAIDs,会带来副作用。中药调经止痛汤(GGD)在治疗 PD 方面显示出了潜力,但确切机制仍不清楚。在这里,我们旨在通过建立大鼠模型来研究 GGD 缓解 PD 的效果,以了解其确切的作用机制。

方法

我们建立了一种由雌二醇和催产素诱导的大鼠痛经模型。将 PD 大鼠每天给予 GGD 或布洛芬(阳性对照)灌胃,连续 7 天。采用酶联免疫吸附试验(ELISA)测定血清中前列腺素 E2(PGE2)、前列腺素 F2α(PGF2α)、β-内啡肽(β-EP)、血栓素 B2(TXB2)、6-酮-前列腺素 F1α(6-keto-PGF1α)的水平。采用免疫组织化学法测定子宫组织中雌激素受体α(ERα)和环氧化酶-2(COX-2)的表达水平,采用 Western blot 分析测定磷酸化和总细胞外信号调节激酶 1 和 2(ERK1/2)的表达水平。

结果

GGD 治疗显著减少了扭体行为、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 增加了β-EP 的含量,并抑制了子宫组织中 ERK1/2 的激活和 ERα 的表达。

结论

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、调节 ERα/ERK1/2/COX-2 通路和增加β-EP 的含量来缓解大鼠的 PD。这些结果为 GGD 治疗 PD 的潜在机制提供了新的认识,并支持将其进一步研究作为治疗 PD 的替代方法。

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