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The anti-inflammatory actions of MUFAs are based on their ability to counteract the effects of long-chain saturated fatty acids on hepatocytes, which include reducing endoplasmic reticulum stress, restricting lipotoxicity induced by accumulation of saturated fatty acids, decreasing ROS production, and inhibiting nuclear factor-B (NF-kB) transcription factors by binding peroxisome proliferator-activated receptor (PPAR) and G-protein coupled surface receptor 120 (GPR120) (138)

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Detoxification Major phase II mechanism via glutathione S-transferases

A hydrogen bond was formed between CDNB and Ala18 residue (Supplementary Figure S2)