| Resumo: |
Over the past few years, AD has been studied as a denomination of neurodegenerative dysfunction, a disease that acts progressively with the accumulation of Beta Amyloid (Aβ). Although the exact cause of AD needs to be further elucidated due to its complexity, growing lines highlight that the accumulation of Aβ protein aggregates is one of the causative events in the pathogenesis of AD. The accumulation of these protein aggregates triggers neuroinflammation, oxidative stress and mitochondrial damage, leading to the loss of neurons. Thus, a great promise is Resveratrol (anti-inflammatory, antioxidant, antitumor and neuroprotective). Therefore, this study aims to evaluate the effects of zein nanoparticles containing resveratrol in an experimental model of neuroinflammation. This is an experimental, descriptive and observational study being carried out in the Neuroanatomy laboratory of the State University of the Center West (UNICENTRO ). Sample consisted of 30 animals divided into control (C), positive control (CP), white nanoparticles (NB), Resveratrol nanoparticles (NR) and resveratrol (R). The animals received 10mg/kg daily, diluted in 0, 5 ml for 15 days. Afterwards, they were submitted to surgery and kept for 30 days for immunohistochemical (IHC) analysis. The results showed that in the qualitative analysis of the IHC, to assess the deposition of Anti Beta Amyloid, there was no change in its morphological brain composition in the NR and C groups, unlike the CP, NB and R groups, which showed changes in the deposition of Anti Tau. it appears that in the NR group there was a normal projection of taurine in the axon which did not correspond in the same way to the other groups, for the CD68 marker in the R and C groups there was no microglial activation. Quantitative analyzes of Anti Beta Amyloid in the NR group showed a statistical difference when compared to the CP, NB and R groups, whereas in the Anti Tau analysis there was a significant difference between the CP and NR groups (p=0.0001), and by end for marker CD68 there was a significant result (p=0.0014) for C and NR. In the analysis of pro and anti-inflammatory cytokines such as IL-10, IL-6, TNF-α and InF-δ that were evaluated by flow cytometry and showing a significant difference in TNF-α between groups C, CP being (p=0.0272) , between group C and NB with the difference of (p=0.0076), CP and NR (p=0.0240) and NB and NR with (p=0.0065), the only group with no statistical difference was the R group. In the analysis of IL-6 and InF -δ showed no significant difference. In IL-10, however, it showed significance between groups C and NR with (p=0.001), group C and R with (p= 0.022) and finally the group CP and NR with a statistical difference being (p=0.0169). It is concluded that NR prevented the evolution of neuroinflammation caused by the induction of beta amyloid1-42 in the hippocampal region CA1. |
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