ABSTRACT
Polycystic ovarian syndrome (PCOS) is an endocrine disorder in women's reproductive age. Currently, the pathophysiology of PCOS is unclear, and the limited treatment options are unsatisfactory. Virgin coconut oil (VCO) is functional food oil associated with pharmacological effects in reproductive disorders. Therefore, we aimed to evaluate whether VCO could enhance clomiphene (CLO) therapy against PCOS in female rats. Rats were randomly divided: (1) Control, (2) PCOS model, (3) PCOS + CLO, (4) PCOS + VCO, and (5) PCOS + CLO + VCO. The PCOS was induced via daily letrozole (1 mg/kg, orally) administration for 21 days. After the PCOS induction, CLO, VCO, and CLO + VCO were administered from days 22 to 36. Serum levels of gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone, estrogen, progesterone, and prolactin were estimated. Polymerase chain reaction gene expression for nuclear factor-erythroid-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), catalase (CAT), glutathione reductase (GSR), LH receptor (LHr), androgen receptor (AR), tumor necrosis factor-alpha (TNF-α), interleukin-1ß (IL-1ß), and caspase-3 were analyzed. The letrozole-induced PCOS caused considerable increases in GnRH, LH, prolactin, estrogen, and testosterone, whereas FSH decreased significantly compared to the control. The gene expression of Nrf2, HO-1, CAT, and GSR were markedly diminished, while IL-1ß, TNF-α, caspase-3, AR, and LHr prominently increased compared to control. Interestingly, the CLO and VCO separately exerted anti-inflammatory and endocrine balance effects. However, VCO-enhanced CLO effect in LH, prolactin and testosterone, Nrf2, HO-1, CAT, GSR, and AR. VCO may synergize with CLO to depress hyperandrogenism and oxidative inflammation in PCOS.
Subject(s)
Polycystic Ovary Syndrome , Animals , Female , Humans , Rats , Caspase 3 , Clomiphene/toxicity , Coconut Oil/toxicity , Estrogens , Follicle Stimulating Hormone , Gonadotropin-Releasing Hormone/pharmacology , Heme Oxygenase-1 , Letrozole/toxicity , Luteinizing Hormone , NF-E2-Related Factor 2/genetics , Polycystic Ovary Syndrome/drug therapy , Prolactin/adverse effects , Testosterone , Tumor Necrosis Factor-alphaABSTRACT
La fluoxetina es un antidepresivo utilizado ampliamente durante varios años. Los efectos secundarios relacionados con la prolactina han sido escasamente detectados. Se plantea un caso clínico de galactorrea inducida por fluoxetina y su evolución dosis-dependiente. (AU)
Subject(s)
Adult , Female , Humans , Galactorrhea/physiopathology , Galactorrhea/complications , Galactorrhea/psychology , Fluoxetine/adverse effects , 26467 , Selective Serotonin Reuptake Inhibitors/pharmacology , Selective Serotonin Reuptake Inhibitors/adverse effects , Prolactin/adverse effects , Prolactin , Anxiety/complications , Anxiety/psychology , Receptors, DopamineSubject(s)
Mental Disorders/blood , Prolactin/blood , Adult , Animals , Bromocriptine/therapeutic use , Drug Synergism , Female , Heart Rate/drug effects , Humans , Hypothalamus/metabolism , Kidney/metabolism , Lithium/pharmacology , Male , Norepinephrine/pharmacology , Osmolar Concentration , Potassium/blood , Premenstrual Syndrome/drug therapy , Prolactin/adverse effects , Prolactin/biosynthesis , Prolactin Release-Inhibiting Factors/metabolism , Rats , Thyrotropin-Releasing Hormone/metabolism , Vascular Resistance/drug effects , Vasoconstrictor AgentsABSTRACT
Prolactin has a cocarcinogenic activity in the rat and mouse as its administration or stimulation of endogenous secretion increases the incidence and reduces the latent period of breast tumours, whether spontaneous or induced by chemical carcinogens. Prolonged hyperprolactinemia obtained by neutralizing the inhibitory influence of the hypothalamus on its secretion and liberation, favours the development of breast carcinoma and inversely. (Estrogens and prolactin exert a synergistic effect, both centrally and peripherally, on the acinar cells of the breast. Prolactin dependency of these mammary carcinomas is due to the persistence of specific cell receptors. In human pathology, it has not yet been possible to demonstrate a comparable effect of prolactin. Radioimmunoassay of plasma prolactin and specific receptors, together with epidemiological enquiries, should rapidly confirm or refute the cocarcinogenic effect of prolactin.