Previous studies demonstrated that depression is more prevalent in women with polycystic ovary syndrome (PCOS). In this study, we aimed to determine whether amitriptyline (AMT), an antidepressant drug, plays a role in preventing PCOS. The results showed that AMT modified ovarian morphology improved the ovarian functions and estrus cycle in estradiol valerate (EV)-induced polycystic ovary (PCO). AMT restored the levels of estradiol (E), testosterone (T) and progesterone (P) to normal, and elevated the level of luteinizing hormone (LH) in EV-induced PCO. No significant changes in follicle stimulating hormone (FSH) levels were observed in rats with EV or AMT treatment. The restoration of norepinephrine (NE) level was detected in rats with EV-induced PCO. AMT also altered the expression levels of steroidogenesis genes and beta2-adrenoceptor (beta2-AR) in EV-induced PCO. Our data revealed that AMT improves the ovarian morphology and modifies ovarian expression of beta2-AR and steroidogenesis genes in rats with EV-induced rat PCO. Our data provide support for the hypothesis that AMT is considered as a candidate drug for preventing and treating PCOS along with depression.
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http://dx.doi.org/10.1007/s12272-015-0573-z | DOI Listing |
Anim Reprod
January 2025
Programa de Pós-graduação em Biotecnologia - PPGBiotec, Universidade Federal do Delta do Parnaíba - UFDPar, Parnaíba, PI, Brasil.
This study aimed to compare the effects of nandrolone decanoate on the morphology and physiology of ovarian tissues in two experimental models, Zebrafish and rats, after in vitro cultivation. A total of 136 animals were used ( rats, n=36, and Zebrafish, n=100). In both experiments, the animals were divided into two groups (Control and Deca) and were exposed to nandrolone decanoate for seven weeks.
View Article and Find Full Text PDFMultiplexed Immunofluorescence (MxIF) enables detailed immune cell phenotyping, providing critical insights into cell behavior within the tumor immune microenvironment (TIME). However, signal integrity can be compromised due to the complex cyclic staining processes inherent to MxIF. Hematoxylin and Eosin (H&E) staining, on the other hand, offers complementary information through its depiction of cell morphology and texture patterns and is often visually cross-referenced with MxIF in clinical settings.
View Article and Find Full Text PDFOncol Res
January 2025
College of Food Sciences, Al-Qasim Green University, Babylon, Iraq.
Cancer, a leading cause of global mortality, remains a significant challenge to increasing life expectancy worldwide. Forkhead Box R2 (FOXR2), identified as an oncogene within the FOX gene family, plays a crucial role in developing various endoderm-derived organs. Recent studies have elucidated FOXR2-related pathways and their involvement in both tumor and non-tumor diseases.
View Article and Find Full Text PDFIUBMB Life
January 2025
Department of Reproductive Medical Center, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.
Abnormality of granulosa cells (GCs) is the critical cause of follicular atresia in premature ovarian failure (POF). RIPK3 is highly expressed in GCs derived from atretic follicles. We focus on uncovering how RIPK3 contributes to ovarian GC senescence.
View Article and Find Full Text PDFCell Commun Signal
January 2025
Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, 100191, China.
Background: Ovarian cancer (OC), particularly high-grade serous ovarian carcinoma (HGSOC), is the leading cause of mortality from gynecological malignancies worldwide. Despite the initial effectiveness of treatment, acquired resistance to poly(ADP-ribose) polymerase inhibitors (PARPis) represents a major challenge for the clinical management of HGSOC, highlighting the necessity for the development of novel therapeutic strategies. This study investigated the role of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), a pivotal regulator of glycolysis, in PARPi resistance and explored its potential as a therapeutic target to overcome PARPi resistance.
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