Lycopene Protects Intestinal Epithelium from Deoxynivalenol-Induced Oxidative Damage via Regulating Keap1/Nrf2 Signaling.

Shahid Ali Rajput,Shao-Jie Liang,Hui-Chao Yan,Xiu-Qi Wang

doi:10.3390/antiox10091493

Shahid Ali Rajput, Shao-Jie Liang + Show 2 more

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https://doi.org/10.3390/antiox10091493

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Abstract

Deoxynivalenol (DON) is a threatening mycotoxin primarily present in the agricultural environment, especially in food commodities and animal forages, and exerts significant global health hazards. Lycopene (LYC) is a potent antioxidant carotenoid mainly present in tomatoes and other fruits with enormous health benefits. The present study was designed to ascertain whether LYC could protect DON-induced intestinal epithelium oxidative injury by regulating Keap1/Nrf2 signaling in the intestine of mice. A total of forty-eight mice were randomly distributed into four groups (n = 12), Control (CON), 10 mg/kg BW LYC, 3 mg/kg BW DON, and 3 mg/kg DON + 10 mg/kg LYC BW (DON + LYC). The experimental groups were treated by intragastric administration for 11 days. Our results showed that LYC significantly increased average daily feed intake (ADFI), average daily gain (ADG), and repaired intestinal injury and barrier dysfunction, as evident by increased trans-epithelial electrical resistance (TEER) and decreased diamine oxidase (DAO) activity, as well as up-regulated tight junction proteins (occludin, claudin-1) under DON exposure. Furthermore, LYC treatment stabilized the functions of intestinal epithelial cells (Lgr5, PCNA, MUC2, LYZ, and Villin) under DON exposure. Additionally, LYC alleviated DON-induced oxidative stress by reducing ROS and MDA accumulation and enhancing the activity of antioxidant enzymes (CAT, T-SOD, T-AOC, and GSH-Px), which was linked with the activation of Nrf2 signaling and degradation of Keap1 expression. Conclusively, our findings demonstrated that LYC protects intestinal epithelium from oxidative injury by modulating the Keap1/Nrf2 signaling pathway under DON exposure. These novel findings could lead to future research into the therapeutic use of LYC to protect the DON-induced harmful effects in humans and/or animals.

Highlights

Food safety is a global challenge to fulfill dire human needs
The in mice, the average daily feed intake (ADFI), average daily gain (ADG), and ADWI were monitored during the experiment
Our results showed that LYC treatment significantly repaired intestinal injury by increasing villus height and crypt depth resulted in better nutrient absorption, suggesting that LYC alleviated DON-induced toxicity on the growth performance of mice

Summary

Introduction

Food safety is a global challenge to fulfill dire human needs. The research impetus is focused on the food contamination caused by the mycotoxins commonly present in the global environment [1,2]. Mycotoxins pose significant harm to human and animal health since they are major hazardous factors contaminating 25% of global crop production [3]. DON is frequently present in the agricultural environment, especially in cereals and animal forages, and causes health hazards to humans and animals [6,7]. Many studies described the deleterious effects of DON on human and animal health, such as food refusal, emesis, growth retardation, immune system, and gastrointestinal tract disorders [8,9]

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