We evaluated the antioxidant activity and neuronal cell-protective effect of fucoidan extract from Ecklonia cava (FEC) on hydrogen peroxide (H 2 O 2 5 0 value = 1.3 mg/ml) and showed a mixed (competitive and noncompetitive) pattern of inhibition. Our findings suggest that FEC may be used as a potential material for alleviating oxidative stress-induced neuronal damage by regulating mitochondrial function and AChE inhibition.
In the present study, we attempt to confirm the effect of the ethyl acetate fraction from Aruncus dioicus var. kamtschaticus (EFAD) against neurodegeneration with various experiments using trimethyltin (TMT). First, learning and memory deterioration caused by TMT was examined with several behavioral tests. EFAD had an improvement effect on TMT‐induced cognitive dysfunction. Second, to assess the oxidative stress caused by TMT, a series of biochemical indicators of the cholinergic and antioxidant system were measured. EFAD showed superb effects on the recovery of the cholinergic system and reduction of oxidative stress. Third, to identify the mitochondrial apoptosis caused by TMT, mitochondrial activity and mitochondrial apoptotic signaling molecules were analyzed. EFAD improved mitochondrial activity and suppressed mitochondrial apoptosis. Finally, dicaffeoylglucose isomers were identified as main compounds of EFAD with ultra‐performance liquid‐quadrupole‐time‐of flight mass spectrometry (UPLC‐QTOF/MS2). Consequently, EFAD showed a protective effect against mitochondrial apoptosis‐induced neurodegeneration in TMT‐injected mice based on antioxidant ability.
Practical applications
Recently, neurodegenerative disease patients are increasing, and in particular, Alzheimer’s disease (AD) is a representative neurodegeneration, which characterized by mitochondrial damage, neurofibrillary tangles, and neuronal cell death. This study confirmed that the ethyl acetate fraction from A. dioicus var. kamtschaticus ameliorates the impaired cognitive ability by TMT toxicity, which shares the symptoms of AD. Therefore, this study can provide the potential of cognitive functional food material of A. dioicus var. kamtschaticus.
An ethyl acetate fraction from Aralia elata (AEEF) was investigated to confirm its neuronal cell protective effect on ethanol-induced cytotoxicity in MC-IXC cells and its ameliorating effect on neurodegeneration in chronic alcohol-induced mice. The neuroprotective effect was examined by methylthiazolyldiphenyl-tetrazolium bromide (MTT) and 2′,7′-dichlorodihydrofluorescein diacetate (DCF-DA) assays. As a result, AEEF reduced alcohol-induced cytotoxicity and oxidative stress. To evaluate the improvement of learning, memory ability, and spatial cognition, Y-maze, passive avoidance, and Morris water maze tests were conducted. The AEEF groups showed an alleviation of the decrease in cognitive function in alcohol-treated mice. Then, malondialdehyde (MDA) levels and the superoxide dismutase (SOD) content were measured to evaluate the antioxidant effect of AEEF in the brain tissue. Treatment with AEEF showed a considerable ameliorating effect on biomarkers such as SOD and MDA content in alcohol-induced mice. To assess the cerebral cholinergic system involved in neuronal signaling, acetylcholinesterase (AChE) activity and acetylcholine (ACh) content were measured. The AEEF groups showed increased ACh levels and decreased AChE activities. In addition, AEEF prevented alcohol-induced neuronal apoptosis via improvement of mitochondrial activity, including reactive oxygen species levels, mitochondrial membrane potential, and adenosine triphosphate content. AEEF inhibited apoptotic signals by regulating phosphorylated c-Jun N-terminal kinases (p-JNK), phosphorylated protein kinase B (p-Akt), Bcl-2-associated X protein (BAX), and phosphorylated Tau (p-Tau). Finally, the bioactive compounds of AEEF were identified as caffeoylquinic acid (CQA), 3,5-dicaffeoylquinic acid (3,5-diCQA), and chikusetsusaponin IVa using the UPLC-Q-TOF-MS system.
Here, we investigated the prebiotic and antioxidant effects of Actinidia arguta sprout water extract (AASWE) on lipopolysaccharide (LPS)-induced cognitive deficit mice. AASWE increased viable cell count, titratable acidity, and acetic acid production in Lactobacillus reuteri strain and showed a cytoprotective effect on LPS-induced inflammation in HT-29 cells. We assessed the behavior of LPSinduced cognitive deficit mice using Y-maze, passive avoidance and Morris water maze tests and found that administration of AASWE significantly improved learning and memory function. The AASWE group showed antioxidant activity through downregulation of malondialdehyde levels and upregulation of superoxide dismutase levels in brain tissue. In addition, the AASWE group exhibited activation of the cholinergic system with decreased acetylcholinesterase activity in brain tissue. Furthermore, AASWE effectively downregulated inflammatory mediators such as phosphorylated-JNK, phosphorylated-NF-κB, TNF-α and interleukin-6. The major bioactive compounds of AASWE were identified as quercetin-3-O-arabinopyranosyl(1 →2)-rhamnopyranosyl(1 →6)-glucopyranose, quercetin-3-O-apiosyl(1 → 2)-galactoside, rutin, and 3-caffeoylquinic acid. Based on these results, we suggest that AASWE not only increases the growth of beneficial bacteria in the intestines, but also shows an ameliorating effect on LPS-induced cognitive impairment.
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