| INTRODUC TI ONMenopause is characterized by many physiological and metabolic changes that can often lead to adverse symptoms in menopausal women; the constellation of these symptoms is known as the climacteric syndrome. This condition can arise due to the decline and reduction of ovarian function in the menopausal transition stage, which can cause hormone secretion imbalance and is likely to induce dysregulation of a series of regulatory and metabolic pathways.The ovaries and uterus are in the recession state during the phase of menopausal transition, and they are the key of studying climacteric syndrome. Accordingly, studying the ageing mechanism of ovary and uterus is important for identifying potential treatment targets. The ageing mechanism is complex; among them, hormone apoptosis, AbstractIn order to investigate the mechanism of genistein (Gen) in the treatment of climacteric syndrome, an in vivo study was performed to investigate the beneficial effects of genistein on the expression of P450 aromatase (P450 arom) and follicle-stimulating hormone receptor (FSHR) in the mouse ovary and uterus. Fifty female ICR mice (45 ± 5g, n = 50), aged 12 months, were divided into the following five groups with 10 animals in each: blank control group (CG), low-dose genistein group (L-Gen), middledose genistein group (M-Gen) and high-dose genistein group (H-Gen) (received 15, 30 and 60 mg/kg of genistein, respectively), and oestrogen group (EG; received 0.5 mg/ kg diethylstilbestrol). The expression levels of the FSHR protein were determined by an immunohistochemical staining method. The expression of P450 arom, Cytochrome P450 19 (CYP19) and FSHR was quantified by real-time PCR. Immunohistochemical results showed that the expression levels of the FSHR protein in the M-Gen (average stained area: 20.79) and the H-Gen (average stained area: 21.21) groups were significantly stronger than in the CG (average area was 17.24) group (p < .05). The expression levels of CYP19 mRNA and P450 arom were positively correlated with the dose of genistein. Specifically, the relative expression levels in the H-Gen and EG groups were more than 1.5 times higher than in the CG group (p < .05). Genistein played a significant role in regulating aromatase and FSHR gene expression to improve perimenopausal ovarian and uterine function. K E Y W O R D S follicle-stimulating hormone receptor, Genistein, menopausal metabolic syndrome model, mice, P450 aromatase How to cite this article: ChuX-L, ZhangT, KongF-X, XiaoY-Y, ChiX-X. The regulatory effect of genistein on P450 aromatase and follicle-stimulating hormone receptor in mouse experimental model of menopausal metabolic syndrome.
The effect of genistein (GEN) on the gene expression level of stromal cell‐derived factor‐1/CXCL‐12 and early growth response gene‐1 was studied in ovarian tissue of young and initially ageing (early stages in the ageing process) female rats. Forty, young female Sprague Dawley (SD) rats of 2–3 months old (200 ±20 g) and forty, initially ageing female SD rats of 10–12 months (490 ± 20 g) old were selected. According to the weight, rats were divided into control group, low‐dose group (L), medium‐dose group (M) and a high‐dose group (H) and were given 15, 30 and 60 mg/kg GEN respectively. The positive control (Oestrogen) group was given 0.5 mg/kg diethylstilbestrol. The treatment lasted for 30 days. The mRNA expression of C‐X‐C motif chemokine ligand 12 (CXCL‐12) and early growth response factor‐1 (EGR‐1) was measured by real‐time PCR, and protein expression of EGR‐1 was detected by Western blot. When compared to the negative control group (NC), the ovary/body weight ratio in the young rats decreased in the GEN group, but the difference was not significant. Similarly, compared with NC, the ovary/body weight ratio in the initially ageing rats also decreased with the increase in GEN concentration, but the decrease was significant in M and H groups (p < .01). The administration of GEN enhanced both the gene and protein expression levels of CXCL‐12 and EGR‐1 in the ovary. Pearson's correlation analysis showed a synergistic effect between CXCL‐12 and EGR‐1. Thus, we conclude that the effect of GEN on CXCL‐12 and EGR‐1 in the initially ageing group was obvious than that in the younger group.
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