Hesperidin ameliorates behavioral impairments and neuropathology of transgenic APP/PS1 mice

Li, Chaoyun; Zug, Caroline; Qu, Hongchun; Schluesener, Hermann J.; Zhang, Zhiyuan

doi:10.1016/j.bbr.2014.12.012

Cited by 80 publications

(37 citation statements)

References 55 publications

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“…7a-c). Recently, Li et al [55] reported that short term hesperidin treatment for 10 days attenuated Ab deposition. However, they did not observe the expression of Ab synthesis related secretases (b and c), which is an interesting outcome, that supports the neuroprotective effect of hesperidin against AD.…”

Section: Discussionmentioning

confidence: 98%

RETRACTED ARTICLE: Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer’s Disease in Wistar Rats

et al. 2015

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The present study was aimed to evaluate the protective effect of hesperidin (Hes) on aluminium chloride (AlCl3) induced neurobehavioral and pathological changes in Alzheimeric rats. Intraperitonial injection of AlCl3 (100 mg/kg body weight) for 60 days significantly elevated the levels of aluminium (Al), activity of acetylcholinesterase (AChE) and protein expressions of amyloid precursor protein (APP), β amyloid (Aβ 1-42), β and γ secretases as compared to control group in hippocampus and cortex of rat brain. Hes administration orally along with AlCl3 injection for 60 days, significantly revert the Al concentration, AChE activity and Aβ synthesis-related molecules in the studied brain regions. Our results showed that aluminum exposure was significantly reduced the spontaneous locomotor and exploratory activities in open field test and enhanced the learning and memory impairments in morris water maze test. The behavioral impairments caused by aluminum were significantly attenuated by Hes. The histopathological studies in the hippocampus and cortex of rat brain also supported that Hes (100 mg/kg) markedly reduced the toxicity of AlCl3 and preserved the normal histoarchitecture pattern of the hippocampus and cortex. From these results, it is concluded that hesperidin can reverse memory loss caused by aluminum intoxication through attenuating AChE activity and amyloidogenic pathway.

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Section: Discussionmentioning

confidence: 98%

RETRACTED ARTICLE: Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer’s Disease in Wistar Rats

et al. 2015

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“…Hesperidin, a flavanone glycoside found abundantly in citrus fruits, was orally given to a transgenic mouse model of cerebral amyloidosis for AD [ 218 ]. Fascinatingly, after a relatively short-term treatment of 10 days, hesperidin significantly restored deficits in non-cognitive nesting ability and social interaction.…”

Section: Neuroprotective Potential Of Polyphenolsmentioning

confidence: 99%

Polyphenols Beyond Barriers: A Glimpse into the Brain

Figueira

Menezes

Macedo

et al. 2017

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BackgroundAgeing can be simply defined as the process of becoming older, which is genetically determined but also environmentally modulated. With the continuous increase of life expectancy, quality of life during ageing has become one of the biggest challenges of developed countries. The quest for a healthy ageing has led to the extensive study of plant polyphenols with the aim to prevent age-associated deterioration and diseases, including neurodegenerative diseases. The world of polyphenols has fascinated researchers over the past decades, and in vitro, cell-based, animal and human studies have attempted to unravel the mechanisms behind dietary polyphenols neuroprotection.MethodsIn this review, we compiled some of the extensive and ever-growing research in the field, highlighting some of the most recent trends in the area.ResultsThe main findings regarding polypolyphenols neuroprotective potential performed using in vitro, cellular and animal studies, as well as human trials are covered in this review. Concepts like bioavailability, polyphenols biotransformation, transport of dietary polyphenols across barriers, including the blood-brain barrier, are here explored.ConclusionThe diversity and holistic properties of polypolyphenol present them as an attractive alternative for the treatment of multifactorial diseases, where a multitude of cellular pathways are disrupted. The underlying mechanisms of polypolyphenols for nutrition or therapeutic applications must be further consolidated, however there is strong evidence of their beneficial impact on brain function during ageing. Nevertheless, only the tip of the iceberg of nutritional and pharmacological potential of dietary polyphenols is hitherto understood and further research needs to be done to fill the gaps in pursuing a healthy ageing.

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“…Some compounds isolated from natural medicine or traditional Chinese medicine such as flavonoids and ginsenosides have been shown beneficial effects against AD (Grundman et al 2002;Dai et al, 2006). Hesperidin (HP), a known flavonoid abundant in citrus, is reported to confer neuroprotective effects (Wang et al 2014;Justin Thenmozhi et al 2015;Li et al 2015), and importantly, it can cross the blood-brain barrier easily (Raza et al 2011;Hwang et al 2012). However, whether HP has neuroprotective effects against AD in vivo and the underlying mechanisms are not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Hesperidin attenuates learning and memory deficits in APP/PS1 mice through activation of Akt/Nrf2 signaling and inhibition of RAGE/NF-κB signaling

Hong

2015

Arch. Pharm. Res.

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Numerous studies have demonstrated that oxidative stress and inflammation play a pivotal role in the pathophysiology of Alzheimer disease (AD). Hesperidin (HP) has various pharmacological effects including anti-oxidative, anti-inflammatory and neuroprotective properties. In this study, APP/PS1 mice were used to evaluate the neuroprotective effects of HP. We reported that intragastric administration of HP (40 mg/kg) for 90 days significantly attenuated cognitive impairment in APP/PS1 mice. HP treatment suppressed oxidative stress by reducing the levels of ROS, LPO, protein carbonyl and 8-OHdG and increasing the activity of HO-1, SOD, catalase, and GSH-Px. HP treatment also inhibited inflammation by decreasing the levels of TNF-α, C-reactive protein and MCP-1 and reducing the activity of NF-κB. Moreover, HP could reverse the decreased phosphorylation of Akt, the decreased phosphorylation of GSK-3β, the lessened Nrf2 and the reduced expression of HO-1. HP could also inhibit the increased the RAGE expression, the enhanced phosphorylation of IκBα, and the augmented nuclear translocation of NF-κB/p65 in cortex of APP/PS1 mice. Taken together, HP suppresses oxidative stress and inflammation via activation of Akt/Nrf2 signaling and inhibition of RAGE/NF-κB signaling and further confers neuroprotection.

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Hesperidin ameliorates behavioral impairments and neuropathology of transgenic APP/PS1 mice

Cited by 80 publications

References 55 publications

RETRACTED ARTICLE: Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer’s Disease in Wistar Rats

RETRACTED ARTICLE: Neuroprotective Effect of Hesperidin on Aluminium Chloride Induced Alzheimer’s Disease in Wistar Rats

Polyphenols Beyond Barriers: A Glimpse into the Brain

Hesperidin attenuates learning and memory deficits in APP/PS1 mice through activation of Akt/Nrf2 signaling and inhibition of RAGE/NF-κB signaling

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