Astaxanthin Alleviates Aflatoxin B1-Induced Oxidative Stress and Apoptosis in IPEC-J2 Cells via the Nrf2 Signaling Pathway.

Toxins (Basel)

Jilin Provincial Key Laboratory of Livestock and Poultry Feed and Feeding in the Northeastern Frigid Area, College of Animal Sciences, Jilin University, Changchun 130062, China.

Published: March 2023

AI Article Synopsis

  • Aflatoxin B1 (AFB1) is a harmful toxin that causes oxidative stress and cell damage, particularly impacting IPEC-J2 cells.
  • Astaxanthin (AST), a potent antioxidant, was found to significantly protect these cells from AFB1-induced toxicity by improving cell viability and reducing biomarkers of oxidative stress and apoptosis.
  • The protective effects of AST are linked to the activation of the Nrf2 signaling pathway, which enhances the expression of antioxidant genes like HO-1 and SOD2.

Article Abstract

Aflatoxin B1 (AFB1), a typical fungal toxin found in feed, is highly carcinogenic. Oxidative stress is one of the main ways it exerts its toxicity; therefore, finding a suitable antioxidant is the key to reducing its toxicity. Astaxanthin (AST) is a carotenoid with strong antioxidant properties. The aim of the present research was to determine whether AST eases the AFB1-induced impairment in IPEC-J2 cells, and its specific mechanism of action. AFB1 and AST were applied to IPEC-J2 cells in different concentrations for 24 h. The AST (80 µM) significantly prevented the reduction in the IPEC-J2 cell viability that was induced by AFB1 (10 μM). The results showed that treatment with AST attenuated the AFB1-induced ROS, and cytochrome C, the Bax/Bcl2 ratio, Caspase-9, and Caspase-3, which were all activated by AFB1, were among the pro-apoptotic proteins which were diminished by AST. AST activates the Nrf2 signaling pathway and ameliorates antioxidant ability. This was further evidenced by the expression of the HO-1, NQO1, SOD2, and HSP70 genes were all upregulated. Taken together, the findings show that the impairment of oxidative stress and apoptosis, caused by the AFB1 in the IPEC-J2 cells, can be attenuated by AST triggering the Nrf2 signaling pathway.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10057844PMC
http://dx.doi.org/10.3390/toxins15030232DOI Listing

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