Hydroxysafflor yellow A exerts beneficial effects by restoring hormone secretion and alleviating oxidative stress in polycystic ovary syndrome mice

• Published in: Experimental physiology 2020-02, Vol.105 (2), p.282-292
• Main Authors: Luo, Man, Huang, Ji‐Cheng, Yang, Zhan‐Qing, Wang, Yu‐Si, Guo, Bin, Yue, Zhan‐Peng
• Format: Article
• Language: English
• Subjects: Antioxidants; Catalase; Cysts; Dehydroepiandrosterone; Endocrine disorders; Estrus cycle; Follicles; Ginsenosides; Glutathione peroxidase; hormone secretion; hydroxysafflor yellow A; Infertility; Luteinizing hormone; Malondialdehyde; Ovaries; Oxidation; Oxidative stress; Polycystic ovary syndrome; Progesterone; Secretion; Superoxide dismutase; Supplements; Testosterone
• ISSN: 0958-0670; 1469-445X
• DOI: 10.1113/EP088147

New Findings What is the central question of this study? What are the potential therapeutic roles of ginsenoside Rb1 and hydroxysafflor yellow A (HSYA) in polycystic ovary syndrome (PCOS). What is the main finding and its importance? HSYA restored the oestrous cycles of PCOS mice, reduced follicular cysts in ovaries and rescued abnormal hormone secretion; ginsenoside Rb1 did not ameliorate the main symptoms of PCOS mice. HSYA alleviated oxidative stress along with an enhancement of antioxidant enzyme activity. This highlights a potential role of HSYA in PCOS therapy. Polycystic ovary syndrome (PCOS) is the most common endocrine disease resulting in female infertility. Hydroxysafflor yellow A (HSYA) and ginsenoside Rb1 have been shown to have antioxidant properties, but little is known about their impact in PCOS. Here dehydroepiandrosterone was used to induce PCOS in a mouse model that was characterized by an irregular oestrous cycle, cystic follicles and an elevated serum testosterone level. Supplementation of HSYA restored the oestrous cycle of PCOS mice, reduced follicular cysts in PCOS mouse ovaries and brought about a decline in serum testosterone level, while ginsenoside Rb1 did not ameliorate the above symptoms of PCOS mice. After HSYA treatment, there was elevation of serum oestradiol, progesterone, luteinizing hormone and anti‐Müllerian hormone levels and a reduction of follicle‐stimulating hormone level, but ginsenoside Rb1 only rescued the levels of follicle‐stimulating hormone and anti‐Müllerian hormone. Further analysis evidenced that HSYA reversed the expression of steroid hormone secretion‐related genes Star, Hsd3b1, Cyp11a1 and Cyp19a1. In PCOS mice HSYA weakened the elevation of ovarian malondialdehyde, which is regarded as a biomarker for oxidative stress. Moreover, HSYA improved reduced glutathione content accompanied by a simultaneous increase in reduced to oxidized glutathione ratio, and enhanced the activities of the antioxidant enzymes superoxide dismutase, glutathione peroxidase and catalase. Collectively, HSYA exerted beneficial effects on PCOS mice by restoring hormone secretion and alleviating oxidative stress.