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Article

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

Department of Animal Nutrition and Feed Sciences, College of Animal Science, South China Agricultural University/Guangdong Laboratory for Lingnan Modern Agriculture/Guangdong Provincial Key Laboratory of Animal Nutrition Control/National Engineering Research Center for Breeding Swine Industry, Guangzhou 540642, China
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Authors to whom correspondence should be addressed.
Academic Editor: Evangelos Zoidis
Antioxidants 2021, 10(9), 1493; https://doi.org/10.3390/antiox10091493
Received: 8 August 2021 / Revised: 11 September 2021 / Accepted: 15 September 2021 / Published: 18 September 2021
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. View Full-Text
Keywords: deoxynivalenol; lycopene; bioactive compound; intestinal injury; oxidative stress; Keap1/Nrf2 signaling deoxynivalenol; lycopene; bioactive compound; intestinal injury; oxidative stress; Keap1/Nrf2 signaling
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MDPI and ACS Style

Rajput, S.A.; Liang, S.-J.; Wang, X.-Q.; Yan, H.-C. Lycopene Protects Intestinal Epithelium from Deoxynivalenol-Induced Oxidative Damage via Regulating Keap1/Nrf2 Signaling. Antioxidants 2021, 10, 1493. https://doi.org/10.3390/antiox10091493

AMA Style

Rajput SA, Liang S-J, Wang X-Q, Yan H-C. Lycopene Protects Intestinal Epithelium from Deoxynivalenol-Induced Oxidative Damage via Regulating Keap1/Nrf2 Signaling. Antioxidants. 2021; 10(9):1493. https://doi.org/10.3390/antiox10091493

Chicago/Turabian Style

Rajput, Shahid A., Shao-Jie Liang, Xiu-Qi Wang, and Hui-Chao Yan. 2021. "Lycopene Protects Intestinal Epithelium from Deoxynivalenol-Induced Oxidative Damage via Regulating Keap1/Nrf2 Signaling" Antioxidants 10, no. 9: 1493. https://doi.org/10.3390/antiox10091493

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