Effects of a Single Dose of Methylprednisolone versus Three Doses of Rosiglitazone on Nerve Growth Factor Levels after Spinal Cord Injury

Effect of carnosine, methylprednisolone and their combined application on irisin levels in the plasma and brain of rats with acute spinal cord injury

“…The animals were randomly divided into 6 experimental groups: Group I (Control, having nothing done, only saline); Group II (sham animals with laminectomy without cross-clamping); Group III (SCI with cross-clamping (Yasargil FE 721); Group IV (SCI with cross-clamping and intraperitoneal administration of carnosine 150 mg/kg and at the first hour and then at 6 h dose regimen of C); Group V (SCI with cross-clamping and ip administration of MP 30 mg/kg) at the first hour and 6 h dose regimen; and Group VI (SCI with cross-clamping and ip administration of C 150 mg/kg) and MP (30 mg/kg) at the first hour and at 6 h dose regimen of C and MP given in the same dose infusion. MP (Meng et al, 2011;Vaquero et al, 2006) and C (Di Paola et al, 2011) doses were chosen according to previously published data in other rat animal experiments. Surgery animals were anesthetized with an ip injection of ketamine (100 mg/kg).…”

PPAR-γ agonist rosiglitazone reduces autophagy and promotes functional recovery in experimental traumaticspinal cord injury

“…The mechanisms of neuroprotection following PPAR-␥ activation include antioxidative properties and anti-inflammatory effects. Additional studies have suggested that ligand-activated PPAR-␥ controls apoptosis, contributes to neuroprotection, and enhances the proliferation of neural progenitor cells [36][37][38][39][40]. It also has been reported that the PPAR-␥ agonist ROSG exerts neuroprotection by inhibiting neuronal autophagy after cerebral ischemia/reperfusion injury [41].…”

Achieving CNS axon regeneration by manipulating convergent neuro-immune signaling

“…In addition to their role in regulating microglia/macrophage function, LXR and PPAR agonists have been shown to confer neuroprotection with improved spontaneous recovery of function in experimental models of SCI Park et al 2007;Paterniti et al 2010;Meng et al 2011). Activation of PPARγ also promotes axonal outgrowth in neuronal cell lines and primary DRG neurons (Miglio et al 2009;Geeven et al 2011), an effect that involves RhoA inhibition (Dill et al 2010).…”

“…In the peripheral nervous system, myelin thickness is reduced in LXR knockout mice, suggesting that LXRs may regulate myelin gene expression (Makoukji et al 2011). A similar role for LXRs has not been proven but in the injured CNS, RXR activation after SCI enhances oligodendrocyte differentiation and remyelination (Meng et al 2011). RXRγ expression has been shown to increase in myelinating Schwann cells, again suggesting a role for type II nuclear receptors in myelination (Latasa and Cosgaya 2011).…”