RESUMO
This study was conducted to determine the effects of glucosamine (GlcN) on zearalenone (ZEA)-induced reproductive toxicity and placental dysfunction in mice. The pregnant mice were randomly divided into one of the four groups, such as the control group, the ZEA group, the GlcN group, and the GlcN plus ZEA group. Reproductive toxicity was induced by consecutive gavages of ZEA at 5 mg/kg body weight during gestational days (GDs 0-14) and in the presence or absence of oral administration of GlcN (0.5 mM). The results showed that GlcN significantly alleviated the decrease of growth performance induced by ZEA exposure of pregnant mice. Meanwhile, ZEA ingestion significantly reduced the number and weight of fetuses, and reduction of placenta weight. Moreover, results of blood biochemical markers indicated that ZEA exposure led to increased oxidative stress levels in pregnant mice. Further analyses demonstrated that ZEA inhibited placental development, resulted in placental inflammation, increased the expression of pro-apoptotic proteins, and decreased the expression of placental tight junction proteins, which were reversed by the administration of GlcN. Results of western blot revealed that GlcN reversed ZEA-mediated phenotype by activating PI3K, while inhibiting MAPK signaling pathway. All these findings showed that GlcN was effective in the protection against ZEA-induced placental dysfunction and reproductive toxicity in pregnant mice. Supplementation of GlcN might be potential nutritional intervention with an ability to alleviate ZEA-induced toxicity in pregnant mice.
