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Previous studies revealed that hepatic oxidative stress was the key mechanism in APAP hepatotoxicity [5, 6] and that up-regulation of PPAR activation by Wy14,643 inhibited fatty acid oxidation after APAP treatment, resulting in suppression of lipid peroxidation and the production of superoxide, the major component of reactive oxygen species (ROS) [16, 22]

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doi: 10.1016/j.bbr.2017.04.038

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