Abstract
Resveratrol can affect the physiology or biochemistry of offspring in the maternal–fetal animal model. However, it exhibits low bioavailability in humans and animals. Fifteen-week SD pregnant female rats were orally administered bisphenol A (BPA) and/or resveratrol butyrate ester (RBE), and the male offspring rats (n = 4–8 per group) were evaluated. The results show that RBE treatment (BPA + R30) compared with the BPA group can reduce the damage caused by BPA (p < 0.05). RBE enhanced the expression of selected genes and induced extramedullary hematopoiesis and mononuclear cell infiltration. RBE increased the abundance of S24-7 and Adlercreutzia in the intestines of the male offspring rats, as well as the concentrations of short-chain fatty acids (SCFAs) in the feces. RBE also increased the antioxidant capacity of the liver by inducing Nrf2, promoting the expression of HO-1, SOD, and CAT. It also increased the concentration of intestinal SCFAs, enhancing the barrier formed by intestinal cells, thereby preventing BPA-induced metabolic disruption in the male offspring rats, and reduced liver inflammation. This study identified a potential mechanism underlying the protective effects of RBE against the liver damage caused by BPA exposure during the peri-pregnancy period, and the influence of the gut microbiota on the gut–liver axis in the offspring.
Highlights
Endocrine disrupting chemicals (EDCs), referred to as environmental hormones, are exogenous compounds that interfere with the endocrine system and demonstrate adverse effects in organisms [1]
We found that the ALT (51.5 U/L) and AST (101.7 U/L) of the bisphenol A (BPA) + R30 groups showed increases of approximately 18% and 37%, respectively, compared with those of the control group, this was significantly lower than that in the BPA groups
The results indicate that supplementation with R30 (RBE) provided full protection against perinatal BPA exposure in the male offspring rats
Summary
Endocrine disrupting chemicals (EDCs), referred to as environmental hormones, are exogenous compounds that interfere with the endocrine system and demonstrate adverse effects in organisms [1]. Studies conducted in Europe and the United States have reported the presence of detectable levels of BPA in more than 90% of urine samples in the general population [4,5,6]. Long-term exposure to BPA may increase the risks of obesity, diabetes mellitus, and breast cancer [7,8]. Previous studies demonstrated the developmental origins of the health and disease (DOHaD) hypothesis [9,10], which highlighted the link between the periconceptual, fetal, and early infant phases of life and the subsequent development of adult obesity and related metabolic disorders [11,12]. Associated research has indicated that exposure to a functional compound may reprogram the adult offspring’s metabolism to cause metabolic syndrome, induced maternally by different medical effects (such as EDCs)
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