Exploring the Toxic Effects of ZEA on IPEC-J2 Cells from the Inflammatory Response and Apoptosis.
Haoyue GuanWenxue MaQiong WuJingzeng CaiZiwei ZhangPublished in: Animals : an open access journal from MDPI (2023)
Zearalenone (ZEA) is the most common fungal toxin contaminating livestock and poultry feeding, especially in pigs, causing severe toxic effects and economic losses. However, the mechanism of ZEA damage to the intestine is unknown. We constructed an in vitro model of ZEA toxicity in a porcine small intestinal epithelial cell (IPEC-J2) line. ZEA causes severe oxidative stress in porcine small intestine cells, such as the production of ROS and a significant decrease in the levels of antioxidant enzymes GSH, CAT, SOD, and T-AOC. ZEA also caused apoptosis in porcine small intestine cells, resulting in a significant reduction in protein and/or mRNA expression of apoptosis-related pathway factors such as P53, caspase 3, caspase 9, Bax, and Cyt-c, which in turn caused a significant decrease in protein and/or mRNA expression of inflammatory-related factors such as IL-1β, IL-2, Cox-2, NF-κD, NLRP3, IL-6, and IL -18, which in turn caused a significant increase in protein and/or mRNA expression levels. The final results suggest that ZEA can cause a severe toxic response in porcine small intestine cells, with oxidative stress, apoptotic cell death and inflammatory damage.
Keyphrases
- oxidative stress
- induced apoptosis
- cell death
- cell cycle arrest
- endoplasmic reticulum stress
- dna damage
- diabetic rats
- ischemia reperfusion injury
- inflammatory response
- signaling pathway
- pi k akt
- early onset
- fluorescent probe
- amino acid
- living cells
- wastewater treatment
- escherichia coli
- lps induced
- anti inflammatory
- quantum dots