Rosiglitazone enhances the proliferation of neural progenitor cells and inhibits inflammation response after spinal cord injury

It has been previously shown that peroxisome proliferators-activated receptor gamma (PPAR-γ) is beneficial for nervous system injury. In present study, we examined the effect of rosiglitazone, a PPAR-γ agonist, on spinal cord injury (SCI) in rats. SCI was induced by dropping a 10 g weight rod at a height of 25 mm. The animals were randomly divided into vehicle group, rosiglitazone treated group, and G3335 treated group. Locomotor function recovery was evaluated by the Basso–Beattie–Bresnahan locomotor rating scale (BBB scale), NF-κB expression and endogenous neural progenitor cells (NPCs) proliferation and differentiation was assessed by flow cytometry and immunohistochemistry. Compared with the vehicle groups, we found that the rosiglitazone could significantly ameliorate locomotor recovery, reduce NF-κB expression, and increase the proliferation of endogenous NPCs. when the PPAR-γ antagonist was use, these effects were abolished. However, neurons differentiating from endogenous NPCs were inhibited when PPAR-γ was activated. Our results suggest that the activation of PPAR-γ may be a potential alternative treatment for spinal cord injury.

► Stimulating PPAR-γ could improve the proliferation of endogenous Neural progenitor cells (NPCs).
► Neither activating nor blocking PPAR-γ pathway improves the endogenous NPC differentiated into neurons.
► TDZ may inhibit the inflammation response in central nervous system (CNS).