engleski

Effects of a PPAR-y agonist, pioglitazone, on the microglia morphology in the traumatic brain injury in the rat

Introduction: Traumatic brain injury (TBI), being one of the leading causes of death and disabilities worldwide, represents an immense problem from a socio-economical and epidemiological aspect. The adequate neuroprotective therapy that could ameliorate neuroinflammation processes is still lacking and in the focus of the preclinical research. A PPAR-γ agonist, pioglitazone, has been shown to attenuate neuronal damage, cortical loss and microglial activation in some rodent models of TBI. Aim of the study: We investigated whether pioglitazone, administered twice daily, affects the microglial morphology as well as the expression of some microglia activation markers in the parietal cortex and the hippocampus of rats following TBI. Materials and methods: Experiments were performed on adult male Wistar rats divided into three groups. Single moderate lateral fluid percussion injury was carried out over the left parietal cortex. Following the injury, animals were administered with pioglitazone or vehicle in the peritoneal cavity in two doses, first one 10 minutes and second 12 hours after injury. Sham-operated, vehicle-treated animals were used as a control group. Twenty-four hours after the injury induction, animals were sacrificed and their brains were extracted and processed for the immunohistological and the Western blot analyses. Results: Digital reconstruction and the analyses of the cells labeled with microglial- specific marker Iba-1 indicated that the brain trauma caused changes in the cellular morphological features such as the extent of the process branching. The application of the tested drug did not affect these morphological changes. However, our results suggest that pioglitazone caused a decrease in the hippocampal expression of TLR- 2, microglia activation marker. Conclusion: Preliminary results of our study imply that pioglitazone could affect some features of the posttraumatic microglial reaction after TBI in the rat. This work was fully supported by project uniri-biomed-18-204 to Ž.G.

microglia ; pioglitazone ; rats ; traumatic brain injury

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