A Novel Multicellular Placental Barrier Model to Investigate the Effect of Maternal Aflatoxin B1 Exposure on Fetal-Side Neural Stem Cells.

Ingestion of food toxins such as aflatoxin B1 (AFB1) during pregnancy may impair fetal neurodevelopment. However, animal model results may not be accurate due to the species' differences, and testing on humans is ethically impermissible. Here, we developed an in vitro human maternal-fetal multicellular model composed of a human hepatic compartment, a bilayer placental barrier, and a human fetal central nervous system compartment using neural stem cells (NSCs) to investigate the effect of AFB1 on fetal-side NSCs. AFB1 passed through the HepG2 hepatocellular carcinoma cells to mimic the maternal metabolic effects. Importantly, even at the limited concentration (0.0641 ± 0.0046 µM) of AFB1, close to the national safety level standard of China (GB-2761-2011), the mixture of AFB1 crossing the placental barrier induced NSC apoptosis. The level of reactive oxygen species in NSCs was significantly elevated and the cell membrane was damaged, causing the release of intracellular lactate dehydrogenase (p < 0.05). The comet experiment and γ-H2AX immunofluorescence assay showed that AFB1 caused significant DNA damage to NSCs (p < 0.05). This study provided a new model for the toxicological evaluation of the effect of food mycotoxin exposure during pregnancy on fetal neurodevelopment.

Myofibrillar protein-chlorogenic acid complexes ameliorate glucose metabolism via modulating gut microbiota in a type 2 diabetic rat model.

Growing evidence suggests that polyphenols could mitigate type 2 diabetes mellitus (T2DM). The glucose-regulatory effects of protein-bound polyphenols, however, have been rarely studied. In this study, macrogenomic and metabolomic analyses were applied to investigate the modulation of myofibrillar protein-chlorogenic acid (MP-CGA) complexes on T2DM rats from the gut microbiota perspective. Results showed that MP-CGA improved hyperglycemia and hyperlipidemia, decreased intestinal inflammation, and reduced intestinal barrier injury. MP-CGA reconstructed gut microbiota in T2DM rats, elevating the abundance of probiotics Bacteroides, Akkermansia, and Parabacteroides while suppressing opportunistic pathogens Enterococcus and Staphylococcus. MP-CGA significantly elevated the concentrations of intestinal metabolites like butyric acid that positively regulate T2DM and reduced the secondary bile acids contents. Therefore, MP-CGA modulated the gut microbiota and related metabolites to maintain stable blood glucose in T2DM rats, providing new insights into the application of protein-polyphenol complexes in foods.