engleski

Effects of pioglitazone on the hippocampus following the experimental traumatic brain injury

Introduction: Traumatic brain injury (TBI) is a major public health concern and one of the leading causes of death and disability worldwide. Recent experimental studies have suggested that peroxisome proliferator-activated receptor gamma (PPARγ) agonists could have neuroprotective effects in in vivo models of TBI. This study was undertaken to evaluate the effects of PPARγ agonist pioglitazone on some parameters of cellular damage and neuroprotection in the hippocampus after brain trauma in the rat. Materials and methods: Moderate TBI was induced using the lateral fluid percussion device and over the left parietal cortex. Ten minutes after the injury induction rats were i.p. injected with either 1 mg/kg pioglitazone or vehicle. Sham- operated, vehicle-treated animals were used as the control group. Rats were sacrificed 24 h following the TBI, their hippocampi were extracted and used for the measurements of the oxidized protein levels, as well as the Western blot analyses of the expressions of cleaved caspase-3, inducible nitric oxide synthase (iNOS), heat shock protein 70 (HSP70), precursor and mature forms of brain derived neurotrophic factor (BDNF). Results: TBI caused a significant caspase-3 activation, an increase in the hippocampal oxidized protein levels and also upregulated precursor BDNF expression, but it had no effect on the iNOS, HSP70 and the mature BDNF expressions. Pioglitazone treatment did not show any effect on the measured parameters levels. Conclusions: In our experimental study, single tested dose of pioglitazone had no evident effects on the hippocampus in the rat TBI model.

Pioglitazone; traumatic brain injury; rat

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