scholarly journals Troxerutin protects against DHT-induced polycystic ovary syndrome in rats

2020 ◽  
Author(s):  
Zixuan Gao ◽  
Xiaochen Ma ◽  
Jing Liu ◽  
Yuhang Ge ◽  
Lei Wang ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Protective Effect ◽  
Rat Model ◽  
Polycystic Ovary ◽  
Body Weight Gain ◽  
Neuroprotective Effect ◽  
The Body ◽  
Reproductive Age ◽  
Ovary Syndrome ◽  
Gonadotrophin Releasing Hormone

Abstract The exact pathogenesis of polycystic ovary syndrome (PCOS), the most common neuroendocrine disorder in women of reproductive age, has not been fully elucidated. Recent studies suggested that chronic inflammation and neurotransmitter disorder involved in the progress of PCOS. Troxerutin, a natural flavonoid, was reported to possess neuroprotective effect in several disease models by inhibiting inflammation or enhancing neurotrophic factor. In this study, we investigated the possible protective effect and mechanism of troxerutin in a dihydrotestosterone (DHT)-induced rat model of PCOS. The PCOS rat models were treated with troxerutin at a dose of 150mg/kg or 300mg/kg for up to 4 weeks. Results showed that 300mg/kg troxerutin significantly decreased the body weight gain and improved the pathological changes of ovary induced by DHT. Meanwhile, the elevated gonadotrophin-releasing hormone (GnRH), gonadotrophin and testosterone in the serum of PCOS rats were reduced with the treatment of troxerutin. The expression of kisspeptin and NKB in arcuate nucleus and their receptors kiss1r and NK3r in GnRH positive neurons of median eminence were markedly decreased in troxerutin-treated rats. Of note, the GnRH inhibitory regulator GABA and stimulatory regulator glutamate were also restored to the normal level by troxerutin. The present study indicated that troxerutin may exhibit a protective effect in PCOS rat model via regulating neurotransmitter release.

scholarly journals Troxerutin protects against DHT-induced polycystic ovary syndrome in rats

2020 ◽  
Author(s):  
Zixuan Gao ◽  
Xiaochen Ma ◽  
Yuhang Ge ◽  
Lei Wang ◽  
Ping Fu ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Protective Effect ◽  
Rat Model ◽  
Polycystic Ovary ◽  
Body Weight Gain ◽  
Neuroprotective Effect ◽  
The Body ◽  
Reproductive Age ◽  
Ovary Syndrome ◽  
Gonadotrophin Releasing Hormone

Abstract The exact pathogenesis of polycystic ovary syndrome (PCOS), the most common neuroendocrine disorder in women of reproductive age, has not been fully elucidated. Recent studies suggested that chronic inflammation and neurotransmitter disorder involved in the progress of PCOS. Troxerutin, a natural flavonoid, was reported to possess neuroprotective effect in several disease models by inhibiting inflammation or enhancing neurotrophic factor. In this study, we investigated the possible protective effect and mechanism of troxerutin in a dihydrotestosterone (DHT)-induced rat model of PCOS. The PCOS rat models were treated with troxerutin at a dose of 150mg/kg or 300mg/kg for up to 4 weeks. Results showed that 300mg/kg troxerutin significantly decreased the body weight gain and improved the pathological changes of ovary induced by DHT. Meanwhile, the elevated gonadotrophin-releasing hormone (GnRH), gonadotrophin and testosterone in the serum of PCOS rats were reduced with the treatment of troxerutin. The expression of kisspeptin and NKB in arcuate nucleus and their receptors kiss1r and NK3r in GnRH positive neurons of median eminence were markedly decreased in troxerutin-treated rats. Of note, the GnRH inhibitory regulator GABA and stimulatory regulator glutamate were also restored to the normal level by troxerutin. The present study indicated that troxerutin may exhibit a protective effect in PCOS rat model via regulating neurotransmitter release.

scholarly journals Troxerutin protects against DHT-induced polycystic ovary syndrome in rats

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Zixuan Gao ◽  
Xiaochen Ma ◽  
Jing Liu ◽  
Yuhang Ge ◽  
Lei Wang ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Protective Effect ◽  
Rat Model ◽  
Polycystic Ovary ◽  
Body Weight Gain ◽  
Neuroprotective Effect ◽  
The Body ◽  
Reproductive Age ◽  
Ovary Syndrome ◽  
Gonadotrophin Releasing Hormone

AbstractThe exact pathogenesis of polycystic ovary syndrome (PCOS), the most common neuroendocrine disorder in women of reproductive age, has not been fully elucidated. Recent studies suggested that chronic inflammation and neurotransmitter disorder involved in the progress of PCOS. Troxerutin, a natural flavonoid, was reported to possess neuroprotective effect in several disease models by inhibiting inflammation or enhancing neurotrophic factor. In this study, we investigated the possible protective effect and mechanism of troxerutin in a dihydrotestosterone (DHT)-induced rat model of PCOS. The PCOS rat models were treated with troxerutin at a dose of 150 mg/kg or 300 mg/kg for up to 4 weeks. Results showed that 300 mg/kg troxerutin significantly decreased the body weight gain and improved the pathological changes of ovary induced by DHT. Meanwhile, the elevated gonadotrophin-releasing hormone (GnRH), gonadotrophin and testosterone in the serum of PCOS rats were reduced with the treatment of troxerutin. The expression of kisspeptin and NKB in arcuate nucleus and their receptors kiss1r and NK3r in GnRH positive neurons of median eminence were markedly decreased in troxerutin-treated rats. Of note, the GnRH inhibitory regulator GABA and stimulatory regulator glutamate were also restored to the normal level by troxerutin. The present study indicated that troxerutin may exhibit a protective effect in PCOS rat model via regulating neurotransmitter release.

scholarly journals The synergistic effect of sex hormone-binding globulin and aromatase genes on polycystic ovary syndrome phenotype.

2008 ◽  
Vol 158 (6) ◽  
pp. 861-865 ◽  
Author(s):  
Nectaria Xita ◽  
Ioannis Georgiou ◽  
Leandros Lazaros ◽  
Vasiliki Psofaki ◽  
George Kolios ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Sex Hormone ◽  
The Body ◽  
Reproductive Age ◽  
Sex Hormone Binding Globulin ◽  
Total Testosterone ◽  
Aromatase Activity ◽  
Hormone Binding ◽  
Ovary Syndrome

ObjectiveExperimental evidence suggests that fetal exposure to androgen excess may program the development of polycystic ovary syndrome (PCOS) in utero. The aim of this study was to examine whether the sex hormone binding globulin (SHBG)(TAAAA)n and the cytochrome P450, family 19 (CYP19)(TTTA)n polymorphisms, known to influence sex hormone-binding globulin (SHBG) levels and aromatase activity respectively, play a synergistic role in the development of PCOS.Design and methodsWe studied 180 women with PCOS and 160 healthy women of reproductive age. The body mass index (BMI) was recorded and the hormonal profile determined from the third to fifth day of menstrual cycle. DNA was extracted from blood leucocytes and the SHBG(TAAAA)n and CYP19(TTTA)n polymorphisms were genotyped.ResultsGenotype analysis revealed 6 SHBG(TAAAA)n alleles with 6–11 repeats and 6 CYP19(TTTA)n alleles with 7–12 repeats. Women were subdivided into four groups: those with short SHBG (≤8 TAAAA repeats) and CYP19 alleles (≤9 TTTA repeats), those with short SHBG–long CYP19 alleles, those with long SHBG–short CYP19 alleles, and those with long SHBG and CYP19 alleles. Women with PCOS tended to have at greater frequency, long SHBG–short CYP19 alleles compared with controls (57.3 vs 42.4%, P=0.07). Importantly, PCOS women with long SHBG–short CYP19 alleles had the lowest SHBG levels (P=0.02) and the highest total testosterone (P=0.008), free androgen index (P=0.002), DHEAS (P=0.02), and testosterone/estradiol ratio (P=0.03), compared with those with other genotypes. This association was independent of age, BMI, and insulin resistance indexes.ConclusionWe speculate that the SHBG and CYP19 genes may have a synergistic role in the developmental programming of PCOS, by affecting androgen bioavailability and aromatization respectively.

scholarly journals Chemerin regulates autophagy to participate in polycystic ovary syndrome

2021 ◽  
Vol 49 (11) ◽  
pp. 030006052110583
Author(s):  
Xiaodong Luo ◽  
Yangyang Gong ◽  
Liuyun Cai ◽  
Lei Zhang ◽  
Xiaojing Dong
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Granulosa Cells ◽  
Rat Model ◽  
Polycystic Ovary ◽  
Mammalian Target Of Rapamycin ◽  
Ectopic Expression ◽  
Reproductive Age ◽  
Ovary Syndrome ◽  
Phosphoinositide 3 Kinase

Objective Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in women of reproductive age. Chemerin has recently been discovered as a novel adipokine associated with obesity and metabolic syndrome. Excessive autophagy activity and overexpression of autophagy-related genes in follicular granulosa cells are important mechanisms of PCOS. This study aimed to investigate the effect of chemerin on autophagy in PCOS. Methods A rat model of PCOS was established by subcutaneous injection of testosterone propionate under a high-fat diet. Expression levels of chemerin and its receptor CMKLR1 were determined by real-time polymerase chain reaction and western blot. Proliferation and apoptosis of human granulosa cells in vitro and expression of autophagy-related genes were examined using bafilomycin A1 (autophagy inhibitor) and Torin1 (autophagy inducer). Results Chemerin and CMKLR1 expression were significantly increased in the ovary in a rat model of PCOS. Ectopic expression of chemerin promoted the proliferation and inhibited the apoptosis of COV434 cells. Ectopic expression of chemerin also induced autophagy by inhibiting the phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway. Conclusions Chemerin and CMKLR1 were overexpressed in PCOS rats. Chemerin promoted autophagy through inhibiting the PI3K/Akt/mTOR pathway, and may provide a potential target and biomarker of PCOS.

scholarly journals Humanin regulates oxidative stress in the ovaries of polycystic ovary syndrome patients via the Keap1/Nrf2 pathway

2020 ◽  
Author(s):  
Yingying Wang ◽  
Nianyu Li ◽  
Zhengyan Zeng ◽  
Li Tang ◽  
Shuhua Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Polycystic Ovary Syndrome ◽  
Pancreatic Beta Cells ◽  
Polycystic Ovary ◽  
Body Weight Gain ◽  
Signalling Pathway ◽  
Reproductive Age ◽  
Related Factor ◽  
Vitamin K3 ◽  
Ovary Syndrome

Abstract Polycystic ovary syndrome (PCOS) is the most common endocrinological pathology among women of reproductive age, whereas the pathogenesis is still not fully understood. Systemic and ovarian oxidative stress (OS) imbalance is a pivotal feature of PCOS. Humanin, a mitochondria-derived peptide, has been reported to function as an antioxidant in cardiomyocytes, pancreatic beta cells and other cells, but how this function is regulated remains unclear. In this study, we investigated whether humanin expression differs in the granulosa cells (GCs) of PCOS patients versus controls, and whether humanin alleviates OS in PCOS ovaries. Sixteen PCOS patients and 28 age- and BMI-matched controls undergoing IVF were recruited, and their serum, follicular fluid and GCs were collected for humanin analysis. Dehydroepiandrosterone-induced rat PCOS models, and vitamin K3-induced OS COV434 cell lines were applied to investigate the mechanism. Humanin expression was significantly down-regulated in the ovaries of PCOS patients relative to those of non-PCOS patients. Exogenous humanin supplementation significantly attenuated body weight gain, ovarian morphological abnormalities, endocrinological disorders and ovarian and systemic OS in PCOS rat models. Our study further demonstrated that this attenuation effect was involved in the modulation of the Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor-erythroid 2-related factor 2 (Nrf2) signalling pathway. In summary, this study reported for the first time that decreased expression of humanin in the GCs was associated with oxidative imbalance in PCOS. Humanin alleviates OS in ovarian GCs of PCOS patients via modulation of the Keap1/Nrf2 signalling pathway.

Humanin alleviates insulin resistance in polycystic ovary syndrome: a human and rat model-based study

Endocrinology ◽  
2021 ◽  
Author(s):  
Yingying Wang ◽  
Zhengyan Zeng ◽  
Shuhua Zhao ◽  
Li Tang ◽  
Jin Yan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Rat Model ◽  
Follicular Fluid ◽  
Polycystic Ovary ◽  
Glucose Consumption ◽  
Cell Types ◽  
Reproductive Age ◽  
Therapeutic Drug ◽  
Ovary Syndrome

Abstract Polycystic ovary syndrome (PCOS), the most common endocrine disorder in women of reproductive age, is characterized by hyperandrogenism and insulin resistance (IR); however, the pathogenesis of local ovarian IR in PCOS remains largely unclear. Humanin, a mitochondria-derived peptide, has been reported to be associated with IR. Our previous study confirmed that humanin is expressed in multiple cell types and is present in follicular fluid. However, it remains unknown whether humanin participates in the pathogenesis of local ovarian IR or whether humanin supplementation can improve IR in PCOS patients. In this study, we compared humanin concentrations in follicular fluid from PCOS patients with and without IR. We further investigated the effect of humanin analogue (HNG) supplementation on IR in a rat model of dehydroepiandrosterone-induced PCOS. Humanin concentrations in the follicular fluid were found to be significantly lower in PCOS patients with IR than in those without IR. HNG supplementation attenuated both the increases in the levels of fasting plasma glucose and fasting insulin in rats with PCOS and the decreases in phosphorylation of IRS1, PI3K, AKT, and GLUT4 proteins in the granulosa cells of these rats. Combined supplementation with HNG and insulin significantly improved glucose consumption in normal and humanin-siRNA-transfected COV434 cells. In conclusion, downregulated humanin in the ovaries may be involved in the pathogenesis of IR in PCOS, and exogenous supplementation with HNG improved local ovarian IR through modulation of the IRS1/PI3K/Akt signaling pathway in a rat model. This finding supports the potential future use of HNG as a therapeutic drug for PCOS.

scholarly journals Yogurt Enriched with Inulin Ameliorated Reproductive Functions and Regulated Gut Microbiota in Dehydroepiandrosterone-Induced Polycystic Ovary Syndrome Mice

Nutrients ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 279
Author(s):  
Tiange Li ◽  
Yue Zhang ◽  
Jiajia Song ◽  
Lijun Chen ◽  
Min Du ◽  
...  
Keyword(s):  
Bile Acid ◽  
Polycystic Ovary Syndrome ◽  
Gut Microbiota ◽  
Polycystic Ovary ◽  
Body Weight Gain ◽  
The Body ◽  
Mice Model ◽  
Ovary Syndrome ◽  
Kegg Pathways ◽  
Bile Acid Profiles

The effects of synbiotic yogurt supplemented with inulin on the pathological manifestations and gut microbiota–bile acid axis were investigated using a dehydroepiandrosterone (DHEA)-induced polycystic ovary syndrome (PCOS) mice model. Female C57BL/6J mice were injected subcutaneously with DHEA at a dose of 6 mg/100 g BW for 20 days to establish a PCOS mouse model. Then, the PCOS mice were treated with yogurt containing inulin (6% w/w) at 15 mL/kg BW for 24 days. Results showed that supplementation of synbiotic yogurt enriched with inulin to PCOS mice decreased the body weight gain, improved estrus cycles and ovary morphology, and reduced the levels of luteinizing hormone while increasing the levels of follicle-stimulating hormone and interleukin-22 in serum. At the genus level, synbiotic yogurt increased the relative abundance of Lactobacillus, Bifidobacterium, and Akkermansia. PICRUSt analysis indicated that KEGG pathways including bile acid biosynthesis were changed after inulin-enriched synbiotic yogurt supplementation. Synbiotic yogurt enriched with inulin also modulated the bile acid profiles. In conclusion, inulin-enriched synbiotic yogurt alleviated reproductive dysfunction and modulated gut microbiota and bile acid profiles in PCOS mice.

Polycystic ovary syndrome and probiotics: a natural approach to an inflammatory disease

2020 ◽  
Vol 16 ◽  
Author(s):  
Antonio Schiattarella ◽  
Gaetano Riemma ◽  
Marco La Verde ◽  
Gianluigi Franci ◽  
Annalisa Chianese ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Critical Role ◽  
Reproductive Age ◽  
Ovary Syndrome ◽  
Natural Approach ◽  
New Treatment ◽  
Gut Microbial Community ◽  
New Evidence

: Polycystic ovary syndrome (PCOS) is a condition that affects about 15% of women of reproductive age and is correlated with infertility, insulin resistance, and obesity. The etiology of PCOS is multifactorial and genetic, endocrine, and metabolic causes were involved. New evidence suggests a link between microorganisms residing in the digestive tracts of humans and the development of PCOS. Moreover, an imbalance in the gut microbial community could be a possible factor for the onset of insulin resistance and obesity. Hyperandrogenism, a key feature of PCOS, could also play a critical role in shaping the microbiome community. Probiotics could modify the gut microbiota and serve as a potential treatment for PCOS. Here we disclose the association between PCOS and intestinal microbiota and the possible role of probiotics as a new treatment approach.

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