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己烯雌酚和缩宫素诱导的原发性痛经导致未孕雌性Wistar大鼠子宫反应性受损。

Primary Dysmenorrhea Induced Using Diethylstilbestrol and Oxytocin Induces Impaired Uterine Reactivity in Virgin Female Wistar Rats.

作者信息

Lacerda-Júnior Francisco Fernandes, da Silva Souza Petruska Pessoa, Ferreira Paula Benvindo, Diniz Anderson Fellyp Avelino, Barros Bárbara Cavalcanti, da Conceição Correia Silva Maria, Alves Adriano Francisco, Silva Alexandre Sérgio, da Silva Bagnólia Araújo

机构信息

Postgraduate Program in Natural and Synthetic Products Bioactives, Health Sciences Center, Federal University of Paraíba, João Pessoa 58051-900, Brazil.

Health Sciences Center, Federal University of Paraíba, João Pessoa 58051-900, Brazil.

出版信息

Pharmaceuticals (Basel). 2025 Aug 13;18(8):1191. doi: 10.3390/ph18081191.

DOI:10.3390/ph18081191
PMID:40872582
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12389008/
Abstract

UNLABELLED

Primary dysmenorrhea (DysP) is a prevalent gynecological condition characterized by painful uterine contractions. However, the underlying mechanism of action of dysmenorrhea has not been fully elucidated. This study aimed to standardize an animal model of dysmenorrhea using diethylstilbestrol and oxytocin to mimic pathophysiological mechanisms in female Wistar rats.

METHODS

For the induction of dysmenorrhea, diethylstilbestrol (s.c.) and oxytocin (i.p.) were used.

RESULTS

The model effectively reproduced hypercontractility and impaired uterine relaxation. The in vivo evaluations demonstrated increased pain responses (DysP group = 119 ± 6.9; control group CG = 3.0 ± 1.0), which were partially attenuated by standard medications (scopolamine/dipyrone and ibuprofen). In vitro assays revealed greater contractile reactivity when compared to that in the control group, in the DysP group, using oxytocin (pEC = 3.6 ± 0.2 and E = 145.1 ± 8.7; CG (pEC = 3.1 ± 0.1 and E = 100%); KCl (DysP pEC = 2.2 ± 0.1 and E = 164 ± 8.0); CG (pEC = 1.8 ± 0.1) and PGF (DysP pEC = 7.4 ± 0.2 and E = 127.3 ± 15.6); CG (pEC = 6.2 ± 0.1)), while the relaxation responses to isoprenaline and nifedipine were decreased compared to those in the CG. The model promoted an imbalance in oxidative stress by increasing malondialdehyde (MDA) levels and reducing the total antioxidant capacity (TAC) in the uterine tissue.

CONCLUSIONS

These findings suggest that the new virgin rat model is capable of replicating key aspects of the clinical features of DysP in humans and offers a valuable tool for studying its pathogenetic mechanisms and testing potential therapeutic agents.

摘要

未标记

原发性痛经（DysP）是一种常见的妇科疾病，其特征为子宫收缩疼痛。然而，痛经的潜在作用机制尚未完全阐明。本研究旨在使用己烯雌酚和缩宫素标准化痛经动物模型，以模拟雌性Wistar大鼠的病理生理机制。

方法

使用己烯雌酚（皮下注射）和缩宫素（腹腔注射）诱导痛经。

结果

该模型有效再现了子宫过度收缩和舒张功能受损。体内评估显示疼痛反应增加（DysP组=119±6.9；对照组CG=3.0±1.0），标准药物（东莨菪碱/安乃近和布洛芬）可部分减轻疼痛反应。体外试验显示，与对照组相比，DysP组使用缩宫素时收缩反应性更高（pEC=3.6±0.2，E=145.1±8.7；CG（pEC=3.1±0.1，E=100%）；氯化钾（DysP pEC=2.2±0.1，E=164±8.0）；CG（pEC=1.8±0.1）和前列腺素F（DysP pEC=7.4±0.2，E=127.3±15.6）；CG（pEC=6.2±0.1）），而异丙肾上腺素和硝苯地平的舒张反应与CG组相比降低。该模型通过增加子宫组织中丙二醛（MDA）水平和降低总抗氧化能力（TAC）促进氧化应激失衡。

结论

这些发现表明，新的未孕大鼠模型能够复制人类DysP临床特征的关键方面，并为研究其发病机制和测试潜在治疗药物提供了有价值的工具。

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