Abstract
Tetragonia tetragonioides (Pall.) Kuntze (TTK) is a medicinal plant traditionally used to treat various diseases such as diabetic, inflammatory, and female-related disorders. Polycystic ovary syndrome (PCOS) is a common endocrinological disorder in women of reproductive age, and hyperandrogenism is a prominent feature of PCOS resulting in anovulation and infertility. In this study, we investigated the effects of a TTK extract on androgen generation and regulation of steroidogenic enzymes in vitro and in vivo. Human adrenocortical NCI-H295R cells were used to assess the effects of TTK extract on production of dehydroepiandrosterone and testosterone, as well as the protein expression of steroidogenic enzymes. Further, a letrozole-induced PCOS rat model was used in vivo to assess whether dietary administration of TTK extract restores normal hormones and reduces PCOS symptoms. TTK extract significantly inhibited forskolin (FOR)-induced androgen production in NCI-H295R cells and serum luteinizing hormone, testosterone, and follicular cysts, but not estradiol, were reduced in letrozole-induced PCOS rats orally administered the TTK extract. In addition, TTK extract inhibits androgen biosynthesis through the ERK-CREB signaling pathway, which regulates CYP17A1 or HSD3B2 expression. TTK extract could be utilized for the prevention and treatment of hyperandrogenism and other types of PCOS.
Highlights
Polycystic ovary syndrome (PCOS) is a common and disturbing endocrine disorder that affects approximately 7% of reproductive-aged women and is characterized by hyperandrogenism, ovulatory dysfunction, insulin resistance, polycystic ovarian morphology on ultrasound, weight gain, hirsutism, and other virilizing signs; hyperandrogenism is the main feature of PCOS [1,2,3,4]
The results of this study show that tetragonioides (Pall.) Kuntze (TTK) extract is an effective inhibitor of androgen biosynthesis, which results from steroidogenic enzymes and ERK-CREB signaling
Because hyperandrogenism is a major pathophysiological feature of PCOS, we examined the excessive androgen generation resulting from hormone imbalances and CYP17A1 and HSD3B2 activity—key enzymes involved in steroidogenesis
Summary
Polycystic ovary syndrome (PCOS) is a common and disturbing endocrine disorder that affects approximately 7% of reproductive-aged women and is characterized by hyperandrogenism, ovulatory dysfunction, insulin resistance, polycystic ovarian morphology on ultrasound, weight gain, hirsutism, and other virilizing signs; hyperandrogenism is the main feature of PCOS [1,2,3,4]. Conditions of hyperandrogenic ovaries as well as adrenal androgen secretion appear to be upregulated in PCOS [2,5]. Excess adrenal androgen levels, especially elevated levels of adrenal androgen metabolites, including dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS), have been reported in ~50% of PCOS patients [5,6,7,8]. Androgen production is necessary for estrogen synthesis, which occurs in all healthy women; hyperandrogenic conditions are characterized by dysfunctional production of androgens. The high levels of luteinizing hormone (LH) observed in common PCOS patients is related to the mechanisms of hyperandrogenism, including exposure of the ovarian theca and granulosa cells to LH and increased levels of cAMP. Stimulation of steroidogenic enzymes leads to the conversion of cholesterol to steroids hormones [1,10]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
