scholarly journals Tilapia Head Protein Hydrolysate Attenuates Scopolamine-Induced Cognitive Impairment through the Gut-Brain Axis in Mice

Foods ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3129
Author(s):  
Jun Ji ◽  
Xiangzhou Yi ◽  
Yujie Zhu ◽  
Hui Yu ◽  
Shuqi Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Cholinergic System ◽  
Hippocampal Neurons ◽  
Dietary Intervention ◽  
Protein Hydrolysate ◽  
Neuroprotective Effect ◽  
Stress System ◽  
Innovative Strategy ◽  
Head Protein

The destruction of the homeostasis in the gut-brain axis can lead to cognitive impairment and memory decline. Dietary intervention with bioactive peptides from aquatic products is an innovative strategy to prevent cognitive deficits. The present study aimed to determine the neuroprotective effect of tilapia head protein hydrolysate (THPH) on scopolamine-induced cognitive impairment in mice, and to further explore its mechanism through the microbiota–gut-brain axis. The results showed that THPH administration significantly improved the cognitive behavior of mice, and normalized the cholinergic system and oxidative stress system of the mice brain. The histopathological observation showed that THPH administration significantly reduced the pathological damage of hippocampal neurons, increased the number of mature neurons marked by NeuN and delayed the activation of astrocytes in the hippocampus of mice. In addition, THPH administration maintained the stability of cholinergic system, alleviated oxidative stress and further improved the cognitive impairment by reshaping the gut microbiota structure of scopolamine-induced mice and alleviating the disorder of lipid metabolism and amino acid metabolism in serum. In conclusion, our research shows that THPH supplementation is a nutritional strategy to alleviate cognitive impairment through the gut-brain axis.

scholarly journals Dexmedetomidine Alleviates Hypoxia-Induced Synaptic Loss and Cognitive Impairment via Inhibition of Microglial NOX2 Activation in the Hippocampus of Neonatal Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Xiaohui Chen ◽  
Dongtai Chen ◽  
Qiang Li ◽  
Shuyan Wu ◽  
Jiahao Pan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Hippocampal Neurons ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Neurological Deficits ◽  
Neonatal Rats ◽  
Synaptic Loss ◽  
Neonatal Hypoxia ◽  
Bv2 Microglia

Background. Perinatal hypoxia is a universal cause of death and neurological deficits in neonates worldwide. Activation of microglial NADPH oxidase 2 (NOX2) leads to oxidative stress and neuroinflammation, which may contribute to hypoxic damage in the developing brain. Dexmedetomidine has been reported to exert potent neuroprotection in several neurological diseases, but the mechanism remains unclear. We investigated whether dexmedetomidine acts through microglial NOX2 to reduce neonatal hypoxic brain damage. Methods. The potential role of microglial NOX2 in dexmedetomidine-mediated alleviation of hypoxic damage was evaluated in cultured BV2 microglia and neonatal rats subjected to hypoxia. In vivo, neonatal rats received dexmedetomidine (25 μg/kg, i.p.) 30 min before or immediately after hypoxia (5% O2, 2 h). Apocynin-mediated NOX inhibition and lentivirus-mediated NOX2 overexpression were applied to further assess the involvement of microglial NOX2 activation. Results. Pre- or posttreatment with dexmedetomidine alleviated hypoxia-induced cognitive impairment, restored damaged synapses, and increased postsynaptic density-95 and synaptophysin protein expression following neonatal hypoxia. Importantly, dexmedetomidine treatment suppressed hypoxia-induced microglial NOX2 activation and subsequent oxidative stress and the neuroinflammatory response, as reflected by reduced 4-hydroxynonenal and ROS accumulation, and decreased nuclear NF-κB p65 and proinflammatory cytokine levels in cultured BV2 microglia and the developing hippocampus. In addition, treating primary hippocampal neurons with conditioned medium (CM) from hypoxia-activated BV2 microglia resulted in neuronal damage, which was alleviated by CM from dexmedetomidine-treated microglia. Moreover, the neuroprotective effect of dexmedetomidine was reversed in NOX2-overexpressing BV2 microglia and diminished in apocynin-pretreated neonatal rats. Conclusion. Dexmedetomidine targets microglial NOX2 to reduce oxidative stress and neuroinflammation and subsequently protects against hippocampal synaptic loss following neonatal hypoxia.

scholarly journals Telomerase increasing compound protects hippocampal neurons from amyloid beta toxicity by enhancing the expression of neurotrophins and plasticity related genes

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Natalie Baruch-Eliyahu ◽  
Vladislav Rud ◽  
Alex Braiman ◽  
Esther Priel
Keyword(s):  
Oxidative Stress ◽  
Amyloid Beta ◽  
Neurotrophic Factors ◽  
Hippocampal Neurons ◽  
Neuroprotective Effect ◽  
Adult Brain ◽  
Beta Catenin ◽  
Adult Mice ◽  
Hippocampal Cell Culture ◽  
Neuronal Degradation

AbstractThe telomerase reverse transcriptase protein, TERT, is expressed in the adult brain and its exogenic expression protects neurons from oxidative stress and from the cytotoxicity of amyloid beta (Aβ). We previously showed that telomerase increasing compounds (AGS) protected neurons from oxidative stress. Therefore, we suggest that increasing TERT by AGS may protect neurons from the Aβ-induced neurotoxicity by influencing genes and factors that participate in neuronal survival and plasticity. Here we used a primary hippocampal cell culture exposed to aggregated Aβ and hippocampi from adult mice. AGS treatment transiently increased TERT gene expression in hippocampal primary cell cultures in the presence or absence of Aβ and protected neurons from Aβ induced neuronal degradation. An increase in the expression of Growth associated protein 43 (GAP43), and Feminizing locus on X-3 genes (NeuN), in the presence or absence of Aβ, and Synaptophysin (SYP) in the presence of Aβ was observed. GAP43, NeuN, SYP, Neurotrophic factors (NGF, BDNF), beta-catenin and cyclin-D1 expression were increased in the hippocampus of AGS treated mice. This data suggests that increasing TERT by pharmaceutical compounds partially exerts its neuroprotective effect by enhancing the expression of neurotrophic factors and neuronal plasticity genes in a mechanism that involved Wnt/beta-catenin pathway.

scholarly journals The neuroprotective effect of Riparin IV on oxidative stress and neuroinflammation related to chronic stress-induced cognitive impairment

2020 ◽  
Vol 122 ◽  
pp. 104758
Author(s):  
Raquell de Castro Chaves ◽  
Auriana Serra Vasconcelos Mallmann ◽  
Natália Ferreira de Oliveira ◽  
Victor Celso Cavalcanti Capibaribe ◽  
Daniel Moreira Alves da Silva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Chronic Stress ◽  
Neuroprotective Effect

scholarly journals NEUROPROTECTIVE EFFECT OF CITRULLUS LANATUS SEED EXTRACTS ON CEREBRAL ISCHEMIC REPERFUSION INJURY INDUCED COGNITIVE IMPAIRMENT AND OXIDATIVE STRESS

2019 ◽  
pp. 38-44
Author(s):  
Girija Pashikanti ◽  
MAKULA AJITHA ◽  
GOVERDHAN PUCHCHAKAYALA
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Citrullus Lanatus ◽  
Neuroprotective Effect ◽  
Memory Performance ◽  
Albino Rats ◽  
Early Event ◽  
Neuroprotective Effects ◽  
Aqueous Fraction ◽  
And Oxidative Stress

Objective: Oxidative stress appears to be an early event involved in the pathogenesis of Alzheimer's disease (AD). The present study was designed to investigate the neuroprotective effects of citrullus lanatus on bilateral common carotid artery occlusion (BCCAO) induced cognitive impairment and oxidative stress in Wistar albino rats. Methods: Cognitive impairment and oxidative stress were induced by BCCAO for 30 min, followed by 7 d reperfusion of male wistar rats. Morris water maze and rectangular maze performance tests and locomotor activity were used to assess memory performance tasks. To study the activity, rats weighing 250-300g were pre-treated with successive extracts of n-hexane fraction (HF), ethyl acetate fraction (EAF), ethanol fraction (EF) and aqueous fraction (AF) of 400 mg/kg, 200 mg/kg, p. o of each for 10 d and the treatment was continued for another 7 d after cerebral ischemia. Various biochemical parameters like lipid peroxidation, Catalase, DPPH and AchE were also estimated in the brain after the treatment. Results: There was significantly increased oxidative stress and cholinesterase activity with cognitive decline in the hippocampus in rats of BCCAO group as compared to sham-operated (p<0.05). The animals treated with Donepezil, HF and EF prevented the biochemical changes significantly (p<0.001) and there was significant (p<0.001) improvement in cognitive parameters compared to BCCAO treated rats. Conclusion: Thus present study indicates the neuroprotective effect of citrulus lanatus seed extract (HF and EF) against BCCAO induced cognitive impairment and associative oxidative damage.

scholarly journals Neuroprotective effect of resveratrol against scopolamine-induced cognitive impairment and oxidative stress in rats

2013 ◽  
Vol 65 (4) ◽  
pp. 1381-1386 ◽  
Author(s):  
Bunadri Pushpalatha ◽  
Neerati Venumadhav ◽  
Merugu Swathi ◽  
Butchi Raju
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Neuroprotective Effect ◽  
And Oxidative Stress
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