Polydatin reduces aflatoxin-B1 induced oxidative stress, DNA damage, and inflammatory cytokine levels in mice

This study showed the protective effect of polydatin (PD), which has an antioxidant activity against oxidative stress in mice caused by aflatoxin B-1 (AFB(1)). In this study, 36 male Swiss albino mice were divided equally into 6 groups: 0.2 mL of FTS was administered to the control group, 0.2 mL of olive oil to the second group, and 0.75 mg/kg AFB(1) to the third group by intragastric gavage every day for 28 days. The fourth, fifth, and sixth groups were administered 50, 100, and 200 mg/kg PD and 0.75 mg/kg AFB(1) intragastrically for 28 days, respectively. AFB(1) administration increased plasma aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, blood urea nitrogen, creatinine, and malondialdehyde levels in blood and tissue samples but decreased the level of glutathione and the activities of superoxide dismutase and catalase. On the other hand, it was determined that PD applications depending on the increasing doses brought these levels closer to normal. In addition, AFB(1) administration increased the amount of ssDNA and liver COX-2, TNF-alpha, IL-6, NF kappa B, and Cyp3a11 mRNA expression levels; on the other hand, it decreased the IL-2 mRNA expression level. In contrast, increasing doses of PD application regulated the amount of ssDNA and these mRNA expression levels. Additionally, histopathological damage was observed in the liver and kidney tissues of the AFB(1) group, while PD applications in a dose-dependent manner improved these damages. As a result, it was determined that PD reduced AFB(1)-induced oxidative stress, DNA damage, and inflammation and exhibited a protective effect on tissues in mice.

Automated summary

This study demonstrates the protective effect of polydatin (PD) against oxidative stress caused by aflatoxin B-1 (AFB(1)) in mice. PD administration at increasing doses effectively reduced oxidative stress, DNA damage, and inflammation induced by AFB(1). Furthermore, PD improved liver and kidney tissue damage caused by AFB(1). These findings highlight the potential of PD as a therapeutic agent against AFB(1)-induced toxicity.