Effects of estrogen-like plant compounds on the vaginal epithelium pituitary, adrenal glands, and uterus of rats.
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ABSTRACT:
SUBMITTER: Mc Rodrigues G
PROVIDER: S-EPMC6384445 | biostudies-literature | 2018 Nov
REPOSITORIES: biostudies-literature
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Effects of estrogen-like plant compounds on the vaginal epithelium pituitary, adrenal glands, and uterus of rats.
Mc Rodrigues Gismar G Db Borges Bruno B Gabriela Q Moreira Leticia L Aparecida G Rossete Érica É de Castro Franca Suzelei S
Experimental biology and medicine (Maywood, N.J.) 20181101 15-16
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Project description:Mitochondrial dynamics plays a significant role in shaping the mitochondrial network and maintaining mitochondrial function. Imbalanced mitochondrial dynamics can cause mitochondrial dysfunction leading to a wide range of diseases/disorders. The aim of this study was to investigate the expression of mitochondrial dynamics markers and regulatory molecules in whole adrenal glands, cortices, and medullae obtained from adult male rats exposed to acute and repeated psychophysical stress, the most common stress in human society. The transcriptional profiles of most of the mitochondrial dynamics markers investigated here were altered: 81%-(17/21) in the whole adrenal gland, 76.2%-(16/21) in the adrenal cortex, and 85.7%-(18/21) in the adrenal medulla. Changes were evident in representatives of every process of mitochondrial dynamics. Markers of mitobiogenesis were changed up to 62.5%-(5/8) in the whole adrenal gland, 62.5%-(5/8) in the adrenal cortex, and 87.5%-(7/8) in the adrenal medulla. Markers of mitofusion were changed up to 100%-(3/3) in the whole adrenal gland, 66.7%-(5/8) in the adrenal cortex, and 87.5%-(7/8) in the adrenal medulla, while all markers of mitofission and mitophagy were changed in the adrenal glands. Moreover, almost all markers of mitochondrial functionality were changed: 83.3%-(5/6) in the whole adrenal, 83.3%-(5/6) in the cortex, 66.7%-(4/6) in the medulla. Accordingly, the study highlights the significant impact of acute and repeated stress on mitochondrial dynamics in the adrenal gland.
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Project description:Background/objectivesDiet-induced obese (DIO) rats have altered stress (HPA) axis activity compared to diet-resistant (DR) rats when chronically exposed to a high-fat (HF) diet. Since stress axis is tightly regulated by leptin, an adipocyte-secreted hormone that is important for controlling body weight, we hypothesized that leptin action is impaired in DIO rats leading to alterations in HPA axis activity.Subjects/methodsWe intraperitoneally injected selectively bred DIO and DR rats with either saline or recombinant rat leptin. HPA axis activity was assessed by measuring norepinephrine (NE) in the paraventricular nucleus (PVN), corticotropin-releasing hormone (CRH) in the median eminence, and serum corticosterone (CORT). To test if HF exposure duration and the corresponding increase in leptin differentially affects HPA axis activity, we placed animals on a chow or HF diet for 1 or 6 weeks.ResultsLeptin injection significantly increased serum leptin levels in both DIO and DR animals. It also reduced PVN NE in both groups, indicating that noradrenergic neurons in both groups remain responsive to leptin. HF diet duration-dependently increased serum leptin only in DIO animals whereas PVN NE increased in both groups. While DR rats responded to HF diet by increasing CRH and CORT at both time-points, responses in DIO rats varied, suggesting that they have altered HPA axis activity that may be dependent on HF-induced leptin levels and/or signaling. To understand the underlying mechanisms, we measured pSTAT-3, a marker of leptin signaling, in brainstem noradrenergic neurons and found reduced pSTAT-3 in A1 region of HF-fed DIO rats. We also found higher serum free fatty acids (FFAs) and a pro-inflammatory cytokine, IL-1β.ConclusionsCollectively, these findings reveal that DIO rats have inherent neuroendocrine impairment in NE-HPA axis circuitry that worsens with the extent of HF diet exposure, possibly due to brainstem leptin resistance and/or elevated circulating FFAs and IL-1β.
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Project description:Estrogens control many aspects of pituitary gland biology, including regulation of lactotroph homeostasis and synthesis and secretion of prolactin. In rat models, these actions are strain specific and heritable, and multiple quantitative trait loci (QTL) have been mapped that impact the responsiveness of the lactotroph to estrogens. One such QTL, Ept7, was mapped to RNO7 in female progeny generated in an intercross between BN rats, in which the lactotroph population is insensitive to estrogens, and ACI rats, which develop lactotroph hyperplasia/adenoma and associated hyperprolactinemia in response to estrogen treatment. The primary objective of this study was to confirm the existence of Ept7 and to quantify the impact of this QTL on responsiveness of the pituitary gland of female and male rats to 17β-estradiol (E2) and diethylstilbestrol (DES), respectively. Secondary objectives were to determine if Ept7 influences the responsiveness of the male reproductive tract to DES and to identify other discernible phenotypes influenced by Ept7. To achieve these objectives, a congenic rat strain that harbors BN alleles across the Ept7 interval on the genetic background of the ACI strain was generated and characterized to define the effect of administered estrogens on the anterior pituitary gland and male reproductive tissues. Data presented herein indicate Ept7 exerts a marked effect on development of lactotroph hyperplasia in response to estrogen treatment, but does not affect atrophy of the male reproductive tissues in response to hormone treatment. Ept7 was also observed to exert gender specific effects on body weight in young adult rats.
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Project description:PURPOSE: The expression of genes regulated by estrogen in the uterus was studied in ovariectomized (OVX) rats treated with germinated brown rice (GBR) bioactives, and compared to Remifemin or estrogen at different doses to identify the regulation of these genes in the uterus and their molecular mechanisms. METHODS: Rats were treated orally with GBR bioactives (phenolics), acylated steryl glucosides (ASG), ?-amino butyric acid (GABA), and ?-oryzanol (ORZ) at 100 and 200 mg/kg, Remifemin (REM) at 10 mg/kg and 20 mg/kg, or estrogen (EST) at 0.2 mg/kg. Ribonucleic acid (RNA) was extracted from the uterus, and messenger (m)RNA expression of selected genes encoding estrogen receptor-beta (ER-?), calcium-binding protein (CaBP9k), complement protein (C3), heat shock protein 70 kDa (HSP70), and interleukin (IL)-4 receptor were quantified. Similarly, serum steroid hormone concentration was monitored at 2, 4, and 8 weeks after treatments. ER-? antibody binding to the uterus sections was also studied using immunohistochemistry. RESULTS: The group treated with EST (0.2 mg/kg) upregulated ER-?, C3, and IL-4 receptor genes compared to other groups (P<0.001). GBR phenolics (200 mg/kg) treatment upregulated the ER-? gene almost to the level of the sham non-treated group. The CaBP9k gene showed upregulation in groups treated with ASG (200 mg/kg), EST (0.2 mg/kg), and ORZ (200 mg/kg) (P<0.05). Estrogen levels increased in groups treated with EST, ASG, and ORZ (200 mg/kg) compared to the OVX untreated group (P<0.05), and there was a slight non-significant decrease (P>0.05) in the progesterone levels in the OVX untreated group compared to the sham and other treated groups. There was a significant increase at 8 weeks in the level of FSH (P<0.05) in the treated groups compared to the OVX untreated group. There was no significant difference (P>0.05) in serum luteinizing hormone (LH) between the OVX untreated group and other groups. The sham and GBR phenolics treated group showed ER-? reactivity at the glandular epithelium, while the group treated with EST showed immunoreactivity at the glandular, luminal, and stromal epithelium. CONCLUSION: GBR phenolics moderately regulate the expression of ER-?, HSP70, and IL-4 receptor genes, and gave a positive immunoreaction to ER-? antigen in the uterus. ASG regulates the expression of CaBP9k and IL-4 receptor genes, and ORZ regulates the expression of the CaBP9k gene, while GABA at 100 mg/kg regulates the expression of the HSP70 gene. GBR and its bioactives might have an effect on estrogen-regulated genes in the uterus of rats.
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Project description:Background and purposeThe functional characterization of secreted peptides can provide the basis for the development of novel therapeutic agents. Augurin is a recently identified secreted peptide of unknown function expressed in multiple endocrine tissues, and in regions of the brain including the hypothalamus. We therefore investigated the effect of hypothalamic injection of augurin on the hypothalamo-pituitary-adrenal (HPA) axis in male Wistar rats.Experimental approachAugurin was given as a single injection into the third cerebral ventricle (i.c.v.) or into the paraventricular nucleus (iPVN) of the hypothalamus. Circulating hormone levels were then measured by radioimmunoassay. The effect of augurin on the release of hypothalamic neuropeptides was investigated ex vivo using hypothalamic explants. The acute effects of iPVN augurin on behaviour were also assessed.Key resultsi.c.v. injection of augurin significantly increased plasma ACTH and corticosterone, compared with vehicle-injected controls, but had no effect on other hypothalamo-pituitary axes hormones. Microinjection of lower doses of augurin into the PVN caused a similar increase in plasma ACTH and corticosterone, without significant alteration in behavioural patterns. Incubation of hypothalamic explants with increasing doses of augurin significantly elevated corticotrophin-releasing factor (CRF) and arginine vasopressin release. In vivo, peripheral injection of a CRF(1/2) receptor antagonist prevented the rise in ACTH and corticosterone caused by i.c.v. augurin injection.Conclusions and implicationsThese data suggest that augurin stimulates the release of ACTH via the release of hypothalamic CRF. Pharmacological manipulation of the augurin system may therefore be a novel target for regulation of the HPA axis.
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Project description:We hypothesize that changes in adrenal gene expression mediate the increased plasma corticosterone and steroidogenesis in rat pups exposed to hypoxia from birth. Keywords: effects of hypoxia on adrenal steroidogenesis in the neonatal rat
2006-11-14 | GSE6249 | GEO