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Persistent inflammation disrupts functional recovery after spinal cord injury (SCI). Peroxisome proliferator-activated receptor gamma (PPAR- γ ) activation promotes functional recovery in SCI rats by inhibiting inflammatory cascades and increasing neuronal survival. We sought to clarify the relationship between PPAR- γ  activation and NACHT, LRR and PYD domain-containing protein 3 (NLRP3) inflammasome suppression, and the role of NF- κ B in activating the NLRP3 inflammasome in neurons. In SCI rats, we found that rosiglitazone (PPAR- γ  agonist) inhibited the expression of caspase-1. In  in vitro  neurons, G3335 (PPAR- γ  antagonist) reversed the rosiglitazone-induced inhibition of caspase-1, interleukin 1 (IL-1 β ), and interleukin 6 (IL-6). Rosiglitazone inhibited the expression of NLRP3, caspase-1, IL-1 β , and IL-6. However, the activator of NLRP3 could counteract this inhibition induced by PPAR- γ  activation. NF- κ B did not participate in the process of rosiglitazone-induced inhibition of NLRP3. Consistent with our  in vitro  results, we verified that locomotor recovery of SCI rats  in vivo  was regulated via PPAR- γ , NLRP3, and NF- κ B. These results suggest that PPAR- γ  activation exerts an anti-inflammatory effect by suppressing the NLRP3 inflammasome—but not NF- κ B—in neurons and that PPAR- γ  activation is a promising therapeutic target for SCI.

PPAR-γ Activation Exerts an Anti-inflammatory Effect by Suppressing the NLRP3 Inflammasome in Spinal Cord-Derived Neurons