褪黑素
氧化应激
自噬
超氧化物歧化酶
活力测定
PI3K/AKT/mTOR通路
过氧化氢酶
蛋白激酶B
细胞生物学
抗氧化剂
化学
生物
药理学
内分泌学
生物化学
细胞凋亡
作者
Yafei Xu,Yunxiao Xie,Zhengchang Wu,Haifei Wang,Zhenhai Chen,Jingneng Wang,Wenbin Bao
标识
DOI:10.1016/j.fct.2023.113803
摘要
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.
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