Protective effects of melatonin on deoxynivalenol-induced oxidative stress and autophagy in IPEC-J2 cells.
Yafei XuYunxiao XieZhengchang WuHaifei WangZhenhai ChenJingneng WangWenbin BaoPublished in: Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association (2023)
This study explored protective effects of melatonin (MEL) on deoxynivalenol (DON)-induced toxicity in porcine jejunum epithelial cells (IPEC-J2). Cells were preexposed to MEL and then exposed to DON to detect cell viability, apoptosis, and oxidative stress indicators. Compared to DON treatment, pretreatment with MEL significantly increased cell proliferation. (P < 0.01), intracellular catalase (CAT) and superoxide dismutase (SOD) levels (P < 0.05), decreased apoptosis and oxidative stress, and significantly attenuated the inflammatory response. RNA-seq analysis revealed that MEL protects IPEC-J2 from the adverse effects of DON by affecting the expression of tight junction and autophagy pathway-related genes. Similarly, further experiments revealed that MEL partly prevented DON-induced disruption of intestinal barrier function and decreased autophagy induced by DON via activation of the AKT/mTOR pathway. In conclusion, these results demonstrated the preventive properties of MEL against DON-induced cell damage by activating the antioxidant system and Inhibition of autophagy.
Keyphrases
- oxidative stress
- diabetic rats
- induced apoptosis
- endoplasmic reticulum stress
- cell cycle arrest
- single cell
- cell death
- rna seq
- cell proliferation
- signaling pathway
- ischemia reperfusion injury
- dna damage
- inflammatory response
- high glucose
- pi k akt
- poor prognosis
- endothelial cells
- lipopolysaccharide induced
- stem cells
- emergency department
- drug induced
- long non coding rna
- mesenchymal stem cells
- heat stress
- adverse drug