PPARγ agonist pioglitazone attenuates cortical neuron lesion and gliosis in rat brain of post-traumatic injury

AIM: To investigate the neuroprotective effect of pioglitazone (Pio), a potent agonist of peroxisome proliferator-activated receptor gamma (PPARγ), on the traumatic brain injury (TBI) in rats. METHODS: SD rats were randomly divided into 4 groups: sham group, vehicle+TBI group, Pio+TBI group and Pio+T0070907+TBI group. TBI was induced by the method of controlled cortical impact (CCI) injury. Neutral red staining technique was used to determine the cortical lesion volume. NeuN, GFAP and OX-42 were measured by immunohistochemical technique to evaluate the morphology of neurons, activation and infiltration of astrocytes and microglia at the edge of cortical lesion. RESULTS: CCI injury in rat elicited activation and proliferation of the astrocytes and microglia. The glial scar wall formation at the edge of cortical lesion, which was accompanied by the loss of neurons, was observed. Pio significantly reduced the cortical lesion volume, the activation and infiltration of the astrocytes and microglia, and the loss of pyramidal neurons at the edge of cortical lesion. T0070907, an antagonist of PPARγ, reversed the effects of Pio. CONCLUSION: Pioglitazone exerts a neuroprotective efficacy, attenuates the loss of neurons and cortical lesion volume following CCI injury by inhibiting the activation and infiltration of astrocytes and microglia, especially glial scar formation.