Neurotransmitter alteration in a testosterone propionate-induced polycystic ovarian syndrome rat model

Chaudhari, Nirja; Nampoothiri, Laxmipriya

doi:10.1515/hmbci-2016-0035

Cited by 25 publications

(19 citation statements)

References 34 publications

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“…However, there was a significant troxerutin-caused (300 mg/kg) decline in hypothalamic GnRH. In regard to the serum hormone levels in rats, many previous studies have reported that LH were generally in the range of 1.5~3 mIU/ml [34,35], FSH levels varied from 8mIU/ml to 20mIU/ml [26,36] and testosterone varied from 0.2 to 10 ng/ml [34,[36][37][38][39], which were approximately consistent with the corresponding results in the present study. Conclusively, troxerutin treatment 300 kg/mg to rats for up to 4 weeks inhibited the hyperactive GnRH/LH system in PCOS rats.…”

Section: Discussionsupporting

confidence: 92%

Troxerutin protects against DHT-induced polycystic ovary syndrome in rats

Gao

Liu

et al. 2020

J Ovarian Res

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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 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.

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Section: Discussionsupporting

confidence: 92%

Troxerutin protects against DHT-induced polycystic ovary syndrome in rats

Gao

Liu

et al. 2020

J Ovarian Res

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show abstract

“…However, there was a significant troxerutin-caused ( 300 mg/kg) decline in serum and hypothalamic GnRH. In regard to the serum hormone levels in rats, many previous studies have reported that LH were generally in the range of 1.5 ~ 3 mIU/ml [32,33], FSH levels varied from 8mIU/ml to 20mIU/ml [22,34]and testosterone varied from 0.2 to 10 ng/ml [32,[34][35][36][37], which were approximately consistent with the corresponding results in the present study. Conclusively, troxerutin treatment 300 kg/mg to rats for up to 4 weeks inhibited the hyperactive GnRH/LH system in PCOS rats.…”

Section: Possession Of Beneficial Effects On Animal Models Of Differesupporting

confidence: 91%

Troxerutin protects against DHT-induced polycystic ovary syndrome in rats

Gao

et al. 2020

Preprint

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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.

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“…However, the concentration and duration of letrozole treatment in that study was much higher as compared to our study. Furthermore, the possibility that the currently observed changes in neurotransmitters are due to other interactions of letrozole can be ruled out by our previous study wherein testosterone propionate-induced PCOS rat model also demonstrated similar neurotransmitter profile [ 67 ]. This thereby strengthens the result of present study indicating that neurotransmitter modulation is a pivotal attribute of PCOS condition.…”

Section: Discussionmentioning

confidence: 99%

GnRH dysregulation in polycystic ovarian syndrome (PCOS) is a manifestation of an altered neurotransmitter profile

Chaudhari

Dawalbhakta

Nampoothiri

2018

Reprod Biol Endocrinol

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BackgroundGnRH is the master molecule of reproduction that is influenced by several intrinsic and extrinsic factors such as neurotransmitters and neuropeptides. Any alteration in these regulatory loops may result in reproductive-endocrine dysfunction such as the polycystic ovarian syndrome (PCOS). Although low dopaminergic tone has been associated with PCOS, the role of neurotransmitters in PCOS remains unknown. The present study was therefore aimed at understanding the status of GnRH regulatory neurotransmitters to decipher the neuroendocrine pathology in PCOS.MethodsPCOS was induced in rats by oral administration of letrozole (aromatase inhibitor). Following PCOS validation, animals were assessed for gonadotropin levels and their mRNA expression. Neurotrasnmitter status was evaluated by estimating their levels, their metabolism and their receptor expression in hypothalamus, pituitary, hippocampus and frontal cortex of PCOS rat model.ResultsWe demonstrate that GnRH and LH inhibitory neurotransmitters – serotonin, dopamine, GABA and acetylcholine – are reduced while glutamate, a major stimulator of GnRH and LH release, is increased in the PCOS condition. Concomitant changes were observed for neurotransmitter metabolising enzymes and their receptors as well.ConclusionOur results reveal that increased GnRH and LH pulsatility in PCOS condition likely result from the cumulative effect of altered GnRH stimulatory and inhibitory neurotransmitters in hypothalamic-pituitary centre. This, we hypothesise, is responsible for the depression and anxiety-like mood disorders commonly seen in PCOS women.

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Neurotransmitter alteration in a testosterone propionate-induced polycystic ovarian syndrome rat model

Cited by 25 publications

References 34 publications

Troxerutin protects against DHT-induced polycystic ovary syndrome in rats

Troxerutin protects against DHT-induced polycystic ovary syndrome in rats

Troxerutin protects against DHT-induced polycystic ovary syndrome in rats

GnRH dysregulation in polycystic ovarian syndrome (PCOS) is a manifestation of an altered neurotransmitter profile

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