Resveratrol Butyrate Esters Inhibit BPA-Induced Liver Damage in Male Offspring Rats by Modulating Antioxidant Capacity and Gut Microbiota

International Journal of Molecular Sciences

Yao-Tsung Yeh¹  Min-Hsi Chiu¹  Yu-Wei Chen²  You-Lin Tain³  Jin-Xian Liao⁴  Chih-Yao Hou⁴  SamK. C. Chang⁵  Ming-Kuei Shih⁶ 

[1] Aging and Disease Prevention Research Center, Fooyin University, Kaohsiung 83102, Taiwan;Department of Medicine, Chang Gung University, Linkow 333, Taiwan;Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan;Department of Seafood Science, National Kaohsiung University of Science and Technology, Kaohsiung 811, Taiwan;Experimental Seafood Processing Laboratory, Costal Research and Extension Center, Mississippi State University, Pascagoula, MS 39567, USA;Graduate Institute of Food Culture and Innovation, National Kaohsiung University of Hospitality and Tourism, 812301 No.1, Songhe Rd., Xiaogang Dist., Kaohsiung 833, Taiwan;

关键词: resveratrol butyrate esters (RBE);    maternal/fetal animal model;    bisphenol A (BPA);    gut microbiota;    short-chain fatty acids (SCFAs);    offspring;   

DOI  :  10.3390/ijms22105273

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown