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

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Publicat a:Pharmaceuticals vol. 18, no. 8 (2025), p. 1191-1209
Autor principal: Lacerda-Júnior, Francisco Fernandes
Altres autors: 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
Publicat:
MDPI AG
Matèries:
Drugs
Hormones
Females
Endometrium
Gynecology
Ischemia
Menstruation
Pathophysiology
Uterus
Hypoxia
Accés en línia:Citation/Abstract
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Resum:Background/Objectives: 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 (pEC50 = 3.6 ± 0.2 and Emax = 145.1 ± 8.7; CG (pEC50 = 3.1 ± 0.1 and Emax = 100%); KCl (DysP pEC50 = 2.2 ± 0.1 and Emax = 164 ± 8.0); CG (pEC50 = 1.8 ± 0.1) and PGF2α (DysP pEC50 = 7.4 ± 0.2 and Emax = 127.3 ± 15.6); CG (pEC50 = 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.
ISSN:1424-8247
DOI:10.3390/ph18081191
Font:Research Library