Astragalus root induces ovarian β‑oxidation and suppresses estrogen‑dependent uterine proliferation.

Abstract

Continuous estrogen stimulation in the uterus has been known to cause excess proliferation of the functional layer of endometrium, resulting in endometrial hyperplasia and leading to infertility. Estrogens can modulate other nuclear receptor signaling pathways, such as peroxisome proliferator‑activated receptors (PPARs). Astragalus root (AsR) has exhibited strong PPARα agonistic activity. Female Imprinting Control Region mice were fed a powder diet that included 5%AsR hot water extract or 0.1% bezafibrate as a positive control for 56days to investigate AsR effects on the reproductive tract, ovary and uterus. AsR resulted in upregulation of the expression of uterine and ovarian PPARα mRNA by 2.5‑fold, and 1.5‑fold, respectively, compared with controls. AsR significantly increased ovarian expression levels of mitochondrial 2,4‑dienoyl‑CoA reductase (mDECR), an auxiliary enzyme involved in β‑oxidation. AsR‑fed mice also exhibited a significant increase in blood estradiol levels and tended to have higher ovary weight. AsR resulted in significantly decreased uterine weight and mDECR expression levels. It has been reported that a PPARα agonist suppresses the development of estrogen‑dependent endometrial hyperplasia. These findings raise the possibility that AsR suppresses estrogen‑dependent endometrial hyperplasia and ovarian dysfunction leading to infertility.