Modulating inflammation is one of the best-studied roles of PPAR activation in astrocytes and has been examined in multiple experimental models (Diab et al., 2002; Giri et al., 2004; Storer et al., 2005a, 2005b; Xu and Drew, 2007; Xu et al., 2007; Lee et al., 2008; Tjalkens et al., 2008; Pineau et al., 2010; Cowley et al., 2012; Hong et al., 2012). In the spinal cord, the PPARγ agonist pioglitazone reduces astrocyte activation in a receptor-dependent manner (Jia et al., 2013). Similarly, the PPARγ agonists 15d-PGJ2 (15-deoxy-Δ-12,14-prostaglandin J-2) and rosiglitazone, and PPARα agonists gemfibrozil and fenofibrate reduced levels of the IL-12 family of cytokines, nitric oxide, IL-6, IL-1β and MCP-1 in primary astrocyte cultures exposed to LPS (Xu and Drew, 2007; Xu et al., 2006, 2007). It is important to note that each drug has different effects on cytokine expression, which can be advantageous since similarly acting drugs can be combined for more potent effects (Diab et al., 2004). Furthermore, attenuating inflammatory signals reduces disease severity in models of MS, even after the onset of clinical symptoms (Diab et al.,
