Role of PPAR in Pain

The first relevance on pain was activation of PPARa in the spinal cord of rats with peripheral inflammation (Benani et al., 2004). Electrophoretic mobility-shift assay was employed to compare the DNA-binding activity toward a PPRE. The PPARa isoform was observed to be activated in the rat spinal cord after complete Freund s adjuvant injection, which could elicit hyperalgesia. PPARa was provided as a new player in the molecular modeling of pain pathways, although it was discussed that inhibitors of PPARa activation might be relevant antinociceptive drugs. 

Thiazolidinediones (TZDs) are potent synthetic agonists of PPARy and medicine for type 2 diabetes. TZDs were shown to induce neuroprotection after cerebral ischemia by blocking inflammation (Culman et al., 2007). Spinal cord injury (SCI), another type of neurodegenerative disease, also induces massive inflammation that precipitates secondary neuronal death. Park et al. (2007) analyzed the therapeutic efficacy of TZDs, pioglitazone, and rosiglitazone, after SCI 

Adachi, M., Kurotani, R., Morimura, K., Shah, Y., Sanford, M., Madison, B. B., Gumucio, D. L., Marin, H. E., Peters, J. M., Young, H. A., and Gosnzalez, F. J. (2006). Peroxisome proliferator activated receptor gamma in colonic epithelial cells protects against experimental inflammatory 

Benani, A., Heurtaux, T., Netter, P., and Minn, A. (2004). Activation of peroxisome proliferator-activated receptor alpha in rat spinal cord after peripheral noxious stimulation. Neurosci. Lett. 369, 

Abdel-Aleem, O. S., Tumber, K. K., Scuderi-Porter, H., and Taylor, B. K. (2008). Intrathecal rosiglitazone acts at peroxisome proliferator-activated receptor-gamma to rapidly inhibit neuropathic pain in rats. J. Pain 9, 639—649. 

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