The inflammation response and risk associated with aflatoxin B1 contamination was minimized by insect peptide CopA3 treatment and act towards the beneficial health outcomes

This study focused on the possible chemo-preventive effects of insect peptide CopA3 on normal human colon cells against the inflammation induced by the toxic environmental pollutant aflatoxin B1 (AFB1). In the study, we used CCD 841 CoN normal human colon cells to investigate the cytotoxic effect induced by AFB1 and elucidated the negative impact of AFB1 exposure on the cell cycle progression. Further, we also carried out the in-vivo experiment, where male BALB/c mice were administrated with AFB1 to induce inflammation associated cancer like phenotype and the dietary effect of CopA3 was evaluated on the early stages of AFB1-induced hepatotoxicity and inflammation in colon tissues. At the initiation stage, CopA3 was given along with water, which significantly decreased the inflammation in the liver and colon of AFB1 exposed mice model. Mice that received CopA3 alone showed enhanced activity of several antioxidant enzymes. In the post treatment stage, the CopA3 dosage remarkably increased the Ki-67 protein expression, indicating the enhancement in cell proliferation event and increased the number of apoptotic cells in colonic crypts, suggesting the capability of CopA3 treatment towards the epithelial cell turnover. Thus, CopA3 treatment shows its potential to inhibit the development of the early stages of AFB1-induced colon inflammation and hepatotoxicity in mice by inhibiting the DNA synthesis of the damaged and inflammatory cell and induced apoptosis for the clearance of damaged cells. Collectively, the results of this study suggest that CopA3 treatment may play a protective role against the mycotoxin induced inflammation. (C) 2020 Elsevier Ltd. All rights reserved.

Automated summary

This study focused on the potential chemo-preventive effects of insect peptide CopA3 on normal human colon cells against inflammation induced by the toxin Aflatoxin B1 (AFB1). The results suggest that CopA3 treatment has the potential to inhibit the development of early stages of AFB1-induced colon inflammation and hepatotoxicity in mice, by inhibiting DNA synthesis of damaged and inflammatory cells and inducing apoptosis for cell clearance.