Resveratrol Butyrate Esters Inhibit BPA-Induced Liver Damage in Male Offspring Rats by Modulating Antioxidant Capacity and Gut Microbiota.
Jin-Xian LiaoYu-Wei ChenMing-Kuei ShihYou-Lin TainYao-Tsung YehMin-Hsi ChiuSam K C ChangChih-Yao HouPublished in: International journal of molecular sciences (2021)
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.
Keyphrases
- high fat diet
- oxidative stress
- diabetic rats
- high glucose
- poor prognosis
- induced apoptosis
- fatty acid
- drug induced
- adipose tissue
- pregnant women
- gene expression
- stem cells
- metabolic syndrome
- dna methylation
- signaling pathway
- cell therapy
- climate change
- long non coding rna
- cell death
- microbial community
- pi k akt
- risk assessment
- cell cycle arrest
- genome wide identification
- cell proliferation
- wastewater treatment
- stress induced
- antibiotic resistance genes
- endoplasmic reticulum stress
- transcription factor
- hematopoietic stem cell