Objective      To determine whether low-dose pioglitazone exerts its neuroprotective effect through peroxisome proliferator-activated receptor gamma (PPARγ)-independent pathway after traumatic brain injury (TBI).        Methods      Thirty 6-week-old male SD rats were randomly divided into sham-injured group

TBI group

T0070907 (antagonist of PPARγ

1.0 mg/kg) group

low-dose pioglitazone group (1.0 mg/kg)

T0070907 (1.0 mg/kg) and pioglitazone  (Pio 1.0 mg/kg) co-administrated group

high-dose Pio group (10.0 mg/kg).  TBI models were established by Feeney free falling method except sham-injured group.  HE

Nissl

TUNEL staining were used to observe the cellular changes

the loss of Nissl body

and the apoptosis of neuronal cells in the brain tissue of experimental rats

and the expression of PPARγ in brain tissue was detected by RT-PCR.        Results      (1) Cellular damage caused by TBI could be reduced after treatment of  low-dose Pio; damage rate of cell in Pio 1.0 group and Pio 10.0 group were less than in T0070907 group and TBI group (P0.05)

while was the same in Pio 1.0 group and  Pio 10.0 group (P0.05). (2) Loss of nissl bodies caused by TBI was reduced after treatment of  low-dose Pioglitazone; loss rates of nissl body in Pio1.0 group and Pio10.0 group were less than in T0070907 group and TBI group (P0.05)

while was the same in Pio 1.0 group and  Pio 10.0 group (P0.05).  (3)Cell apoptosis induced by TBI was reduced after treatment of  low-dose Pio; apoptosis cell number  in Pio 1.0 group and Pio 10.0 group was less than in T0070907 group and TBI group (P0.05)

while was the same in Pio 1.0 group and  Pio10.0 group (P0.05).  (4) PPARγ  mRNA expressed highest in  Pio 10.0 group

which had significant difference with Pio 1.0 group (P0.05).        Conclusion      Low-dose Pio exerts  neuroprotection through the PPARγ-independent pathway after TBI

which plays an important part on treating TBI.