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Bisphenol P exposure in C57BL/6 mice caused gut microbiota dysbiosis and induced intestinal barrier disruption via LPS/TLR4/NF-κB signaling pathway
https://orcid.org/0000-0003-0311-7856
https://orcid.org/0000-0003-0593-397X
Graphical abstract Display Omitted
Highlights Different BPP exposure concentrations and different exposure durations altered the gut microbiota diversity and structural composition. M (30 µg/kg body weight (BW)/day) and H (3000 µg/kg BW/day) groups exposed to BPP displayed an intestine inflammatory response. M and H groups exposed to BPP experienced disruption of the intestinal barrier. M and H groups exposed to BPP experienced bacterial translocation and endotoxemia. An antibiotic combination alleviated intestinal inflammation and barrier disruption due to gut microbiota dysbiosis.
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.
Bisphenol P exposure in C57BL/6 mice caused gut microbiota dysbiosis and induced intestinal barrier disruption via LPS/TLR4/NF-κB signaling pathway
https://orcid.org/0000-0003-0311-7856
https://orcid.org/0000-0003-0593-397X
Graphical abstract Display Omitted
Highlights Different BPP exposure concentrations and different exposure durations altered the gut microbiota diversity and structural composition. M (30 µg/kg body weight (BW)/day) and H (3000 µg/kg BW/day) groups exposed to BPP displayed an intestine inflammatory response. M and H groups exposed to BPP experienced disruption of the intestinal barrier. M and H groups exposed to BPP experienced bacterial translocation and endotoxemia. An antibiotic combination alleviated intestinal inflammation and barrier disruption due to gut microbiota dysbiosis.
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.
Bisphenol P exposure in C57BL/6 mice caused gut microbiota dysbiosis and induced intestinal barrier disruption via LPS/TLR4/NF-κB signaling pathway
https://orcid.org/0000-0003-0311-7856
https://orcid.org/0000-0003-0593-397X
Graphical abstract Display Omitted
Highlights Different BPP exposure concentrations and different exposure durations altered the gut microbiota diversity and structural composition. M (30 µg/kg body weight (BW)/day) and H (3000 µg/kg BW/day) groups exposed to BPP displayed an intestine inflammatory response. M and H groups exposed to BPP experienced disruption of the intestinal barrier. M and H groups exposed to BPP experienced bacterial translocation and endotoxemia. An antibiotic combination alleviated intestinal inflammation and barrier disruption due to gut microbiota dysbiosis.
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.
Bisphenol P exposure in C57BL/6 mice caused gut microbiota dysbiosis and induced intestinal barrier disruption via LPS/TLR4/NF-κB signaling pathway
Ma, Nana (author) / Ma, Diao (author) / Liu, Xia (author) / Zhao, Lining (author) / Ma, Lei (author) / Ma, Dan (author) / Dong, Sijun (author)
2023-04-20
Article (Journal)
Electronic Resource
English