학술논문

Resveratrol directly affects ovarian cell sirtuin, proliferation, apoptosis, hormone release and response to follicle-stimulating hormone (FSH) and insulin-like growth factor I (IGF-I).
Document Type
Article
Source
Reproduction, Fertility & Development. 2019, Vol. 31 Issue 8, p1378-1385. 8p.
Subject
*LUTEINIZING hormone releasing hormone
*SOMATOMEDIN C
*GONADOTROPIN
*RESVERATROL
*APOPTOSIS
*CELL physiology
Language
ISSN
1031-3613
Abstract
The objective of our study was to examine the influence of the plant polyphenol resveratrol (R) on the rapamycin signalling pathway (mammalian target of rapamycin; mTOR) and basic ovarian cell functions in mammalian targets, as well as on their response to the physiological hormonal stimulators follicle-stimulating hormone (FSH) and insulin-like growth factor I (IGF-I). Resveratrol was found to stimulate sirtuin 1 accumulation and apoptosis, inhibit proliferation, suppress P and promote T and E release. Alone, FSH promoted proliferation and had no effect on apoptosis, but had an inhibitory effect on these processes when combined with R. IGF-I alone stimulated proliferation and inhibited apoptosis and promoted P production but not that of T; however, in the presence of R, the addition of IGF-I switched from having an anti-apoptotic to a pro-apoptotic effect and stimulated T release, but it did not modify the effect of IGF-I on proliferation and P output. These observations: (1) demonstrate that R directly affects the basic ovarian cell functions of proliferation, apoptosis and steroidogenesis, (2) provide further evidence of the involvement of FSH and IGF-I in the regulation of these processes, (3) demonstrate the ability of R to prevent and even invert the effects of FSH and IGF-I on ovarian cells and (4) indicate that the effects of R may be mediated by the mTOR–sirtuin intracellular signalling system. This study aimed to examine whether the plant polyphenol resveratrol (R) can directly affect ovarian functions. The present observations: (1) demonstrate that R directly affects ovarian cell proliferation, apoptosis and steroidogenesis, (2) provide further evidence of the involvement of FSH and IGF-I in the regulation of these processes, (3) demonstrate the ability of R to prevent and even invert the effects of FSH and IGF-I on ovarian cells and (4) indicate that the effects of R may be mediated by the mTOR–sirtuin intracellular signalling system. [ABSTRACT FROM AUTHOR]