Bisphenol P exposure in C57BL/6 mice caused gut microbiota dysbiosis and induced intestinal barrier disruption via LPS/TLR4/NF-κB signaling pathway

Abstract

Despite being one of the most world's widely used and mass-produced compounds, bisphenol A (BPA) has a wide range of toxic effects. Bisphenol P (BPP), an alternative to BPA, has been detected in many foods. The effects of BPP dietary exposure on gut microbiota and the intestinal barrier were unclear. We designed three batches of animal experiments: The first studied mice were exposed to BPP (30 µg/kg BW/day) for nine weeks and found that they gained weight and developed dysbiosis of the gut microbiota. The second, using typical human exposure levels (L, 0.3 µg/kg BW/day BPP) and higher concentrations (M, 30 µg/kg BW/day BPP; H, 3000 µg/kg BW/day BPP), caused gut microbiota dysbiosis in mice, activated the Lipopolysaccharide (LPS) /TLR4/NF-κB signaling pathway, triggered an inflammatory response, increased intestinal permeability, and promoted bacterial translocation leading to intestinal barrier disruption. The third treatment used a combination of antibiotics and alleviated intestinal inflammation and injury. This study demonstrated the mechanism of injury and concentration effects of intestinal damage caused by BPP exposure, providing reference data for BPP use and control and yielding new insights for human disease prevention.

Keywords

• BPP
• BPA analogues
• Gut microbes
• Intestinal barrier function