Ginsenoside Rg1 ameliorates reproductive function injury in C57BL/6J mice induced by di-N-butyl-phthalate.

With the aggravation of environmental pollution, the incidence of infertility is increasing. Ginsenoside Rg1 is a monomer component extracted from Panax ginseng. It has been found that Ginsenoside Rg1 is able to prevent premature ovarian failure and delay testicular senescence. Therefore, we speculate Ginsenoside Rg1 may have great potential to prevent and treat infertility. The aim of this work is to explore whether Ginsenoside Rg1 plays a protective role in the dinbutyl phthalate (DBP)-induced reproductive function injury mice, and to elucidate the potential mechanism. C57BL/6J male mice were administered by DBP with or without Ginsenoside Rg1 treatment and serum, testis and epididymis were collected for further analysis. Sperm analysis, hematoxylin and eosin staining, and serum hormone detection indicated that Ginsenoside Rg1 treatment improved the sperm density and sperm motility, reduced the testicular tissue damage, increased the serum testosterone and luteinizing hormone levels, and decreased the serum follicle-stimulating hormone level in DBP-induced mice. Furthermore, Ginsenoside Rg1 treatment upregulated expression levels of spermatogenesis-related protein, Cx43, E-cadherin, p-PI3K, p-Akt, and mTOR in the mice treated by DBP, observed by using a immunohistochemistry assay, a real-time quantitative PCR assay, and a western blot analysis. The present study reveals that Ginsenoside Rg1 may exert anti-DBP-induced reproductive function injury in C57BL/6J mice. In addition, the protect role of Ginsenoside Rg1 in spermatogenesis may be associated with the regulation of reproductive hormones, upregulation of spermatogenic associated proteins expression, restoration of the gap junctions, and the activation of PI3K/Akt/mTOR signaling pathways.

Intrauterine exposure to low-dose DBP in the mice induces obesity in offspring via suppression of UCP1 mediated ER stress.

Dibutyl phthalate (DBP) is recognized as an environmental endocrine disruptor that has been detected in fetal and postnatal samples. Recent evidence found that in utero DBP exposure was associated with an increase of adipose tissue weight and serum lipids in offspring, but the precise mechanism is unknown. Here we aimed to study the effects of in utero DBP exposure on obesity in offspring and examine possible mechanisms. SPF C57BL/6J pregnant mice were gavaged with either DBP (5 mg /kg/day) or corn oil, from gestational day 12 until postnatal day 7. After the offspring were weaned, the mice were fed a standard diet for 21 weeks, and in the last 2 weeks 20 mice were selected for TUDCA treatment. Intrauterine exposure to low-dose DBP promoted obesity in offspring, with evidence of glucose and lipid metabolic disorders and a decreased metabolic rate. Compared to controls, the DBP exposed mice had lower expression of UCP1 and significantly higher expression of Bip and Chop, known markers of endoplasmic reticulum (ER) stress. However, TUDCA treatment of DBP exposed mice returned these parameters nearly to the levels of the controls, with increased expression of UCP1, lower expression of Bip and Chop and ameliorated obesity. Intrauterine exposure of mice to low-dose DBP appears to promote obesity in offspring by inhibiting UCP1 via ER stress, a process that was largely reversed by treatment with TUDCA.