Abstract
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-1β 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.
Highlights
The offspring were kept with the mother rat until weaning at the postnatal day 21 (PND21), and all procedures were performed by experimenters trained in animal handling
MDA levels in the hippocampus revealed an increase in lipoperoxidation in the HI + Sal group as compared to controls (F(3.17) = 15.81 p < 0.001), and this effect was prevented in the HI + Plinia trunciflora fruit extract (PTE) group (p < 0.05); on the other hand, in the cerebral cortex, high lipoperoxidation levels were not prevented by PTE (F(3.16) = 5.733, p < 0.05)
No significant differences were observed between MAD levels among groups when striatum was analyzed (F(3.16) = 0.1257, p > 0.05). These findings indicate that HI causes lipid damage in the hippocampus and cerebral cortex, and that PTE prevented lipoperoxidation in these structures
Summary
Neonatal hypoxia–ischemia (HI) is one of the main causes of injuries affecting the Central Nervous System (CNS) in neonates [1]. HI is caused by gestational complications or events that occur after birth [1,2] and promotes unfavorable conditions for brain development, which contribute to the emergence of motor and cognitive impairments, emotional disorders, and various neurological diseases [3]. The pathophysiology of HI is caused by oxygen deprivation and the interruption of blood flow to the brain tissue [1,4]. Low concentrations of substrates such as glucose and oxygen lead to metabolic failure and the reduction of Adenosine Triphosphate (ATP)
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