RESUMO
<b>Background and Objective:</b> Cerebellar fluorosis is a health issue associated with excessive exposure to fluoride (F) either in direct or indirect ways as pesticides, drinking water and caries preventing prescriptions. It is characterized by elevation in oxidative stress, inflammation, demyelination and Purkinje cell loss. <i>Moringa oleifera</i> (M), is a widely cultivated plant used as a health-booster agent in modulating various disorders because of its high content of vitamins and minerals. The beneficial effect of moringa against fluoride-induced cerebellar toxicity in pregnant rats was investigated in this study. <b>Materials and Methods:</b> Twenty pregnant rats were administered daily 300 mg kg<sup></sup><sup>1</sup> <i>M. oleifera</i> aqueous extract incorporated with 10 mg kg<sup></sup><sup>1</sup> of F intoxication from the 1st day of gestation until the 20th day. Following the termination of the trial, sera were collected and cerebellar tissue was removed for further examinations, along with the assessment of maternity. <b>Results:</b> The <i>M. oleifera</i> significantly normalized serum FSH, LH, progesterone, dopamine and serotonin levels of F-intoxicated mothers. Additionally, <i>M. oleifera</i> markedly prevented the lipid peroxidation and DNA fragmentation indicated by the tail length and moment in comet assay (-34.4 and -75.3%, respectively, when compared to the fluoride intoxicated group), while sustaining the levels of SOD and CAT revealing its antioxidant activity. The <i>M. oleifera</i> regressed the cerebellar α-amylase (-25.4%) and acetylcholinesterase activity (-40.6%), also attenuated GFAP (-73.4%, p<0.0001), synaptophysin level (216.6%, p<0.0001) and IL-6 expression (-91.2%) comparing to fluoride only treated mothers. <b>Conclusion:</b> Histological and ultrastructural examinations confirmed the recuperating effects of <i>M. oleifera</i> on mothers' cerebellar tissue intoxicated with fluoride indicated by intact folia and restored Purkinje cells number and architecture. The maternal study emphasized the anti-abortifacient activity of moringa against fluoride induced-fetotoxicity.
Assuntos
Moringa oleifera , Humanos , Gravidez , Ratos , Feminino , Animais , Moringa oleifera/química , Árvores , Fluoretos/farmacologia , Sinaptofisina/farmacologia , Acetilcolinesterase , Estresse Oxidativo , Extratos Vegetais/farmacologia , Extratos Vegetais/químicaRESUMO
In this study, we investigated the anti-amnesic effect of Korean red pine (Pinus densiflora) bark extract (KRPBE) against amyloid beta1-42 (Aß1-42)-induced neurotoxicity. We found that treatment with KRPBE improved the behavioral function in Aß-induced mice, and also boosted the antioxidant system in mice by decreasing malondialdehyde (MDA) content, increasing superoxide dismutase (SOD) activities, and reducing glutathione (GSH) levels. In addition, KRPBE improved the cholinergic system by suppressing reduced acetylcholine (ACh) content while also activating acetylcholinesterase (AChE), regulating the expression of choline acetyltransferase (ChAT), postsynaptic density protein-95 (PSD-95), and synaptophysin. KRPBE also showed an ameliorating effect on cerebral mitochondrial deficit by regulating reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and ATP levels. Moreover, KRPBE modulated the expression levels of neurotoxicity indicators Aß and phosphorylated tau (p-tau) and inflammatory cytokines TNF-α, p-IκB-α, and IL-1ß. Furthermore, we found that KRPBE improved the expression levels of neuronal apoptosis-related markers BAX and BCl-2 and increased the expression levels of BDNF and p-CREB. Therefore, this study suggests that KRPBE treatment has an anti-amnestic effect by modulating cholinergic system dysfunction and neuroinflammation in Aß1-42-induced cognitive impairment in mice.
Assuntos
Disfunção Cognitiva , Fármacos Neuroprotetores , Pinus , Acetilcolina/metabolismo , Acetilcolina/farmacologia , Acetilcolinesterase/metabolismo , Trifosfato de Adenosina/metabolismo , Peptídeos beta-Amiloides , Animais , Antioxidantes/farmacologia , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Colina O-Acetiltransferase/metabolismo , Colina O-Acetiltransferase/farmacologia , Colinérgicos/farmacologia , Disfunção Cognitiva/induzido quimicamente , Disfunção Cognitiva/tratamento farmacológico , Glutationa/metabolismo , Malondialdeído/metabolismo , Malondialdeído/farmacologia , Camundongos , Inibidor de NF-kappaB alfa/metabolismo , Doenças Neuroinflamatórias , Fármacos Neuroprotetores/farmacologia , Estresse Oxidativo , Casca de Planta , Extratos Vegetais/farmacologia , Espécies Reativas de Oxigênio/metabolismo , República da Coreia , Superóxido Dismutase/metabolismo , Sinaptofisina/metabolismo , Sinaptofisina/farmacologia , Fator de Necrose Tumoral alfa/metabolismo , Proteína X Associada a bcl-2/metabolismoRESUMO
BACKGROUND: During the elderly, hippocampal neurogenesis and synaptogenesis reduce and dark neurons (DNs) increase, leading to cognitive impairment. It is believed that natural products can protect the neural cells and system by protecting from damages or promoting regeneration. Therefore, the effects of grape seed extract (GSE) on the hippocampus of aged mice were investigated in this study. METHODS: twelve old mice were divided into two groups of control and GSE. Animals in the GSE group received 300â mg/kg of GSE for eight weeks via gavage. At the end of treatment, cognition performance was evaluated by Morris water maze (MWM) and passive avoidance tests. Hippocampal neurogenesis, synaptogenesis and DNs production were evaluated with immunohistochemistry and histological evaluations on 5-micron coronal tissue sections. RESULTS: The hippocampal mean number of double cortin positive cells (DCX+) per unit area, as well as synaptophysin expression in the GSE group, were significantly higher than the control group (p < 0.01). The frequency of DNs in the GSE group was lower than the control group (p < 0.05). Behavioral tests showed that GSE improves memory and learning performance. CONCLUSION: Consuming GSE in the elderly can potentially alleviate the age-related reduction of hippocampal neurogenesis and synaptogenesis. It is also able to decrease hippocampal DNs production and increase memory and learning.