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It is suggested that these side effects are due to mitochondrial dysfunction, decreased antioxidant activity, and induction of inflammatory and apoptotic mediators

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Notably, PPAR alone is not sufficient to restore redox homeostasis and promote the M2 phenotype, as demonstrated by the exacerbation of neuroinflammatory cytokine production in NRF2-deficient mice challenged with LPS (Innamorato et al., 2008)