Ameliorative effects of canolol against acrylamide toxicity in PC12 cells through modulating MAPKs pathway and autophagy

Abstract

Acrylamide (ACR), widely present in heat treatment of starchy foods, has attracted much attention in chronic neurotoxin. Canolol is a crucial phenolic compound and generated in rapeseed oil during microwave pressing. The present study aimed to reveal the ameliorative effects of canolol against ACR-induced toxicity in PC12 cells and the underlying mechanism. Cells pretreated with canolol inhibited ACR-exerted cytotoxicity and cell apoptosis. Canolol attenuated the increase of intracellular ROS and MDA level induced by ACR, and restored ACR-triggered depletion of glutathione content and mitochondrial membrane potential. Furthermore, canolol upregulated expressions of phosphorylated ERK1/2 protein, and downregulated phosphorylated p38 and JNK proteins after 24 h pretreatment in ACR-treated PC12 cells. Notably, ACR-stimulated autophagy activation was hindered by canolol in counteracting ACR-exerted LC-3 conversion and promoting the expression of p62 protein. Our study demonstrated that canolol prevented ACR damage involving MAPKs pathway and autophagy in PC12 cells, providing a potential application of canolol for ACR toxicity.

Keywords

• Acrylamide
• Toxicity
• Canolol
• MAPKs
• Autophagy