4.7 Article

Dihydroartemisinin alleviates deoxynivalenol induced liver apoptosis and inflammation in piglets

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出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2022.113811

关键词

Apoptosis; Deoxynivalenol; Dihydroartemisinin; Inflammation; Liver; Piglet

资金

  1. Natural Science Foundation of Heilongjiang Province [TD2019C001]
  2. State Key Program of Na- tional Natural Science Foundation of China [32030101]
  3. Science and Technology Development Program of Jilin Province [20210202039NC]

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In this study, the effects of DHA on liver apoptosis and inflammation induced by DON in piglets were investigated. Results showed that DHA improved the negative effects of DON on serum biochemical parameters, inflammatory cytokine levels, hepatic antioxidant capacity, hepatic apoptosis, and inflammation.
Deoxynivalenol (DON) is one of the mycotoxins that contaminate cereals and feed, thereby endangering human and animal health. Dihydroartemisinin (DHA), a derivative of artemisinin, has anti-inflammatory and antioxi-dant functions in addition to anti-malaria and anti-cancer. The purpose of this study was to investigate the effects of DHA on alleviating liver apoptosis and inflammation induced by DON in piglets. The experimental design followed a 2 (normal diet and DON-contaminated diet) x 2 (with and without supplementation of DHA) factorial arrangement. 36 weaned piglets were subjected to a 21-day experiment. Results showed that DON increased ALT activity, the levels of TNF-alpha, IL-1 beta and IL-2, and reduced the levels of total protein (TP) and albumin (ALB) in the serum. However, DHA decreased the levels of TNF-alpha, IL-1 beta and IL-2, and increased the levels of TP and ALB. Also, DON decreased glutathione (GSH) content and catalase (CAT) activity, and increased methane dicarboxylic aldehyde (MDA) content. But GSH content was increased by DHA. In addition, DHA decreased DON-induced increase in apoptosis rate of hepatocytes. Furthermore, DON activated death receptor pathway to promote apoptosis by up-regulating the protein expression of FasL and caspase-3, and the mRNA expression of FasL, TNFR1, caspase-8, Bid, Bax, CYC and caspase-3. However, DHA reduced caspase-3 protein expression, as well as the mRNA expression of FADD, Bid, Bax, CYC and caspase-3. Besides, DON also activated TNF/NF-kappa B pathway to induce an inflammatory response by up-regulating TNF-alpha protein expression, and the mRNA expression of TNFR1, RIP1, IKK beta, I kappa B alpha, IL-1 beta and IL-8. Nevertheless, DHA reduced the mRNA expression of RIP1, I kappa B alpha, NF-kappa B, IL-1 beta and IL-6, and the protein expression of TNF-alpha and NF-kappa B. In conclusion, DHA improved DON-induced negative effects on serum biochemical parameters and inflammatory cytokine levels, hepatic antioxidant ca-pacity, hepatic apoptosis and inflammation.

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