Quercetin ameliorates learning and memory via the Nrf2-ARE signaling pathway in d-galactose-induced neurotoxicity in mice

Dong, Fuxing; Wang, Shuang; Wang, Yiwen; Yang, Xiao; Jiang, Jiali; Wu, Dejian; Qu, Xuebin; Fan, Huiying; Yao, Ruiqin

doi:10.1016/j.bbrc.2017.07.151

Cited by 85 publications

(50 citation statements)

References 39 publications

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“…It seems important to note that the neuroprotective effect of HO-1 induction is mainly due to the Nrf2-dependent activation, as widely discussed earlier in this review. In ageing as well, for instance, there is evidence that the Nrf2-dependent HO-1 up-regulation due to the treatment with flavonoids or carotenoids is protective against galactose-induced ageing-like neurodegeneration [110,111] and that voluntary running, through the up-regulation of HO-1, improves age-related cognitive decline in rats [112]. The role played by Nrf2 in ageing and neurodegenerative diseases has been widely reviewed elsewhere and there is a general agreement on the fact that in older organisms there is a decline of Nrf2 activity [113].…”

Section: Ho-1 Up-regulation In Neurodegenerationmentioning

confidence: 99%

Heme Oxygenase 1 in the Nervous System: Does It Favor Neuronal Cell Survival or Induce Neurodegeneration?

Nitti

Piras

Brondolo

et al. 2018

IJMS

123

107

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Heme oxygenase 1 (HO-1) up-regulation is recognized as a pivotal mechanism of cell adaptation to stress. Under control of different transcription factors but with a prominent role played by Nrf2, HO-1 induction is crucial also in nervous system response to damage. However, several lines of evidence have highlighted that HO-1 expression is associated to neuronal damage and neurodegeneration especially in Alzheimer’s and Parkinson’s diseases. In this review, we summarize the current literature regarding the role of HO-1 in nervous system pointing out different molecular mechanisms possibly responsible for HO-1 up-regulation in nervous system homeostasis and neurodegeneration.

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Section: Ho-1 Up-regulation In Neurodegenerationmentioning

confidence: 99%

Heme Oxygenase 1 in the Nervous System: Does It Favor Neuronal Cell Survival or Induce Neurodegeneration?

Nitti

Piras

Brondolo

et al. 2018

IJMS

123

107

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“…Chronic high dose D-gal causes significant decrease in step-through latency and significant increase time in the dark indicating deterioration of memory and cognitive skills (Zhong et al, 2016) which could be due to increase osmotic pressure with cell swelling and membrane lipid impairment with nerve degeneration caused by galactitol one of metabolites of D-gal (Wei et al, 2017) .D-gal may also results in neurological damage by Aβ accumulation ( Dong et al, 2017).…”

Section: Discussion:-mentioning

confidence: 99%

Study the Effect of Silibinin on Experimentally Induced Memory Impairment in Male Rats.

HamdyBasha¹,

AhmedElsawy²,

MohamedMady³

et al. 2018

IJAR

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Aim of the work: is to study the effect of different doses of silibinin on D-galactose induced memory impairment in male rats. Methods:60 male rats were divided into four groups, the first three groups were (10 rats each) and the fourth group (30 rats) was subdivided in to three subgroups (10 rats each)I-Control group was injected subcutaneously by physiological saline once daily for six weeks II-D-galactose group was injected subcutaneously by 150 mg/kg of D-galactose once daily for six weeks III-Placebo group 10 ml/kg of 0.5 % carboxymethylcellulose solution was injected intraperitonealy once daily for six weeks IV-Silibinin group include IVa(2 mg/kg),IVb(20mg/kg),IVc(200 mg/kg), silibinin was suspended in 10ml/kg of 0.5 % carboxymethylcellulose solution and injected intraperitonealy once daily for six weeks. Results: D-galactose group produced significant decrease step-through latency, increase time in the dark and increase in tissue malondialdehyde, nitrite, acetylcholine esterase, tumor necrosis factoralpha level and caspase activity, it produced significant decrease in tissue catalase activity and brain-derived neurotrophic factor level when compared to control group.There was insignificant change in placebo group and silibinin (2 mg/kg) when compared to D-galactose group.While, it produced significant change in silibinin (20 mg/kg) and (200 mg/kg) when compared to placebo group, but it still produced significant change in silibinin (20 mg/kg) and silibinin (2 mg/kg) when compared to control group,it produced insignificant change in silibinin (200 mg/kg) when compared to control group. Conclusion: Silibinin has role in memory disorders which develops efficient therapeutic approaches.

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“…As the literature review of animal studies shows, several mechanisms have been suggested as to the possible positive mechanism of quercetin's effects on memory, including the activation of the ERK/CREB/BDNF, Nrf2‐ARE, Akt, AMPK signaling pathways or NMDA receptors, and the inhibition of the Ask/JNK/Jun, RAGE signaling pathway, and PP2Cα (Dong et al., ; Liu et al., ; Martínez de Morentin et al., ; Pei et al., ; Tongjaroenbuangam et al., ; Xia et al., ). Refer to Figure for more details on the potential signaling pathways of quercetin.…”

Section: Quercetin and Memorymentioning

confidence: 99%

“…There are several animal models of AD, and memory impairment including amyloid β (Aβ) (Facchinetti, Bronzuoli, & Scuderi, 2018), the transgenic mouse model of AD (Wang et al, 2014), lipopolysaccharide (Wang et al, 2018), and the streptozotocin (STZ) (Bhutada et al, 2010), scopolamine (Nouriziabari et al, 2018), D-galactose (Dong et al, 2017), hypoxia (Prasad et al, 2013), and ischemia models (Viswanatha et al, 2015). quercetin can affect its absorption (D'Andrea, 2015).…”

Section: Introductionmentioning

confidence: 99%

Quercetin in Food: Possible Mechanisms of Its Effect on Memory

Babaei

Mirzababaei

Nassiri‐Asl

2018

Journal of Food Science

102

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Quercetin (3,3',4',5,7-pentahydroxyflavone) is found in vegetables and fruits. It is one of the major flavonoids that is part of human diets. Quercetin has several pharmacological effects in the nervous system as a neuroprotective agent. In this review, we summarize the research on quercetin and its role in memory in both animals and humans. Articles were chosen from the Scopus, PubMed, and Web of Science databases. In this review, we describe and summarize the importance of quercetin's presence in the body, particularly in the brain; its kinetics, including its absorption, metabolism, distribution, and excretion; its behavioral effects; and some of the possible mechanisms of action of quercetin on memory in different animal models. Several important pathways that may be involved in the processes of learning and memory, long-term potentiation, and cognition may be impaired during neurological diseases or other medical conditions. As dietary quercetin is important, provision of its best formulation for delivery to the brain as a nutraceutical and in clinical translational research for the prevention or treatment of Alzheimer's disease and other types of dementia is necessary.

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Quercetin ameliorates learning and memory via the Nrf2-ARE signaling pathway in d-galactose-induced neurotoxicity in mice

Cited by 85 publications

References 39 publications

Heme Oxygenase 1 in the Nervous System: Does It Favor Neuronal Cell Survival or Induce Neurodegeneration?

Heme Oxygenase 1 in the Nervous System: Does It Favor Neuronal Cell Survival or Induce Neurodegeneration?

Study the Effect of Silibinin on Experimentally Induced Memory Impairment in Male Rats.

Quercetin in Food: Possible Mechanisms of Its Effect on Memory

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