Plinia trunciflora Extract Administration Prevents HI-Induced Oxidative Stress, Inflammatory Response, Behavioral Impairments, and Tissue Damage in Rats

The disruption of redox homeostasis and neuroinflammation are key mechanisms in the pathogenesis of brain hypoxia-ischemia (HI); medicinal plants have been studied as a therapeutic strategy, generally associated with the prevention of oxidative stress and inflammatory response. This study evaluates the neuroprotective role of the Plinia trunciflora fruit extract (PTE) in neonatal rats submitted to experimental HI. The HI insult provoked a marked increase in the lipoperoxidation levels and glutathione peroxidase (GPx) activity, accompanied by a decrease in the brain concentration of glutathione (GSH). Interestingly, PTE was able to prevent most of the HI-induced pro-oxidant effects. It was also observed that HI increased the levels of interleukin-1 beta in the hippocampus, and that PTE-treatment prevented this effect. Furthermore, PTE was able to prevent neuronal loss and astrocyte reactivity induced by HI, as demonstrated by NeuN and GFAP staining, respectively. PTE also attenuated the anxiety-like behavior and prevented the spatial memory impairment caused by HI. Finally, PTE prevented neural tissue loss in the brain hemisphere, the hippocampus, cerebral cortex, and the striatum ipsilateral to the HI. Taken together our results provide good evidence that the PTE extract has the potential to be investigated as an adjunctive therapy in the treatment of brain insult caused by neonatal hypoxia-ischemia.

Automated summary

This study demonstrates that the Plinia trunciflora fruit extract (PTE) has a neuroprotective role in neonatal rats with experimental brain hypoxia-ischemia (HI). PTE effectively prevents oxidative stress and inflammatory response induced by HI, as evidenced by reduced lipoperoxidation levels and interleukin-1 beta levels. PTE also prevents neuronal loss, astrocyte reactivity, anxiety-like behavior, spatial memory impairment, and neural tissue loss caused by HI.