Role of Toll-like Receptor/MyD88 Signaling in Lycopene Alleviated Di-2-ethylhexyl Phthalate (DEHP)-Induced Inflammatory Response

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作者
Dai, Xue-Yan [1 ,4 ]
Zhu, Shi-Yong [1 ]
Chen, Jian [1 ]
Li, Mu-Zi [1 ]
Talukder, Milton [1 ,5 ]
Li, Jin-Long [1 ,2 ,3 ]
机构
[1] College of Veterinary Medicine, Northeast Agricultural University, Harbin,150030, China
[2] Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin,150030, China
[3] Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, Northeast Agricultural University, Harbin,150030, China
[4] Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang,330045, China
[5] Department of Physiology and Pharmacology, Faculty of Animal Science and Veterinary Medicine, Patuakhali Science and Technology University, Barishal,8210, Bangladesh
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This study has received support from the National Natural Science Foundation of China (No. 32172932); the Key Program of Natural Science Foundation of Heilongjiang Province of China (No. ZD2021C003); the China Agriculture Research System of MOF and MARA (No. CARS-35); the Distinguished Professor of Longjiang Scholars Support Project (No. T201908); and the Heilongjiang Touyan Innovation Team Program;
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摘要
Lycopene (Lyc) has anti-inflammatory and antioxidant biological functions. Di-2-ethylhexyl phthalate (DEHP) is an extremely harmful and persistent environmental pollutant and is a threat to animal health. The toll-like receptor (TLR)/MyD88 pathway is an important pathway in the inflammatory response. To illustrate the potential antagonistic action of Lyc against DEHP by the TLR/MyD88 pathway, 140 ICR mice were randomly assigned groups and continuously gavaged with corn oil, distilled water, different DEHP concentrations (500 or 1000 mg/kg BW/day), and/or Lyc (5 mg/kg BW/day) for 28 days. The data show that Lyc effectively attenuates the DEHP-induced activation of the TLR/MyD88 pathway, the upregulation of JNK expression, the content of IL-6 and TNF-α, and the downregulation of the IL-10 content, which eventually inhibit the inflammatory response and mitochondrial injuries. These findings underline the TLR/MyD88 pathway as a potential therapeutic target in DEHP and Lyc as a new therapeutic method to inhibit DEHP toxicity. © 2022 American Chemical Society.
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页码:10022 / 10030
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