Inhibition of β-Amyloid Aggregation by Albiflorin, Aloeemodin and Neohesperidin and their Neuroprotective Effect on Primary Hippocampal Cells Against β-Amyloid Induced Toxicity

Ho, See‐Lok; Poon, Chung‐Yan; Lin, Cheng Yuan; Yan, Ting; Kwong, Daniel W. J.; Yung, Kin Lam; Wong, Man; Bian, Zhaoxiang; Li, Hung‐Wing

doi:10.2174/1567205012666150504144919

Cited by 46 publications

(19 citation statements)

References 17 publications

(18 reference statements)

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“…Additionally, hesperidin has been shown to have a preventive effect against neuronal cell death that likely involves the PI3 and MAP kinase pathways 52 . Finally, hesperidin has been shown to reduce excitotoxicity and ROS levels 53 . The current study confirms that hesperidin can reduce oxidative stress and prevent RGC death in vivo , suggesting that hesperidin has potential as a new antioxidant supplement to prevent the degeneration of the RGCs in various retinal diseases.…”

Section: Discussionmentioning

confidence: 99%

The neuroprotective effect of hesperidin in NMDA-induced retinal injury acts by suppressing oxidative stress and excessive calpain activation

Maekawa

Sato

Fujita

et al. 2017

Sci Rep

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We found that hesperidin, a plant-derived bioflavonoid, may be a candidate agent for neuroprotective treatment in the retina, after screening 41 materials for anti-oxidative properties in a primary retinal cell culture under oxidative stress. We found that the intravitreal injection of hesperidin in mice prevented reductions in markers of the retinal ganglion cells (RGCs) and RGC death after N-methyl-D-aspartate (NMDA)-induced excitotoxicity. Hesperidin treatment also reduced calpain activation, reactive oxygen species generation and TNF-α gene expression. Finally, hesperidin treatment improved electrophysiological function, measured with visual evoked potential, and visual function, measured with optomotry. Thus, we found that hesperidin suppressed a number of cytotoxic factors associated with NMDA-induced cell death signaling, such as oxidative stress, over-activation of calpain, and inflammation, thereby protecting the RGCs in mice. Therefore, hesperidin may have potential as a therapeutic supplement for protecting the retina against the damage associated with excitotoxic injury, such as occurs in glaucoma and diabetic retinopathy.

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Section: Discussionmentioning

confidence: 99%

The neuroprotective effect of hesperidin in NMDA-induced retinal injury acts by suppressing oxidative stress and excessive calpain activation

Maekawa

Sato

Fujita

et al. 2017

Sci Rep

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“…EMO has been testified to be a neoteric type of anticancer drug with selective activity against neuro-ectodermal cancers [24]. More importantly, a growing number of researches have corroborated that EMO might be a neuroprotective agent for remedy nervous system diseases [17,25]. Cerebral ischemia injury belongs to central nervous system (CNS) injury, which gives rise to irreversible brain damage and even neurological sequelae [26].…”

Section: Discussionmentioning

confidence: 99%

Emodin relieves hypoxia-triggered injury via elevation of microRNA-25 in PC-12 cells

Cao¹,

Fang

Jia

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Emodin (EMO) possesses extensive pharmacological activities, which has been proven to exert the protective impact in diverse nervous system diseases. Nonetheless, whether EMO emerges a neuro-protective activity in hypoxic-evoked ischemic brain injury is still further probed. The intention of the research is to disclose whether EMO emerges neuro-protective activity in hypoxic-evoked ischemic brain injury. PC-12 received hypoxia administration, and then cell viability, apoptosis and autophagy were estimated. After EMO disposition, the above-involved cellular processes were evaluated again. MiR-25 functions in EMO-affected cells were also estimated. The interrelation between miR-25 and neurofilament light-chain polypeptide gene (NEFL) and the conceivable roles of NEFL in hypoxia-disposed cells were investigated. The latent mechanism was uncovered by mTOR and Notch pathways determination. Hypoxia triumphantly triggered apoptosis and autophagy, but EMO repressed these functions in PC-12 cells. Increased miR-25 was induced by EMO, and inhibited miR-25 abated the impacts of EMO on hypoxia-disposed PC-12 cells. NEFL as a neoteric target gene of miR-25 was predicated, and overexpressed NEFL annulled the functions of EMO in hypoxia-injured cells. EMO activated mTOR and Notch pathways through repressing NEFL. The investigations corroborated that EMO weakened hypoxia-triggered injury via elevating miR-25 by targeting NEFL in PC-12 cells.

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“…DSS decreased the content of arginine vasopressin (AVP) in the pituitary and the expression of AVP mRNA in hypothalamus [42]. In addition, albiflorin can maintain the intracellular Ca 2+ concentration [86] (Fig. 1).…”

Section: The Effect On the Neurotransmitter And The Central Nervous Smentioning

confidence: 96%

“…Albiflorin reduced the toxicity and ROS induced by both monomeric and oligomeric Aβ species to exhibit a potent inhibitory effect on Aβ1-40 and Aβ1-42 aggregation. In addition, albiflorin can maintain the intracellular Ca 2+ concentration [86].…”

Section: Figure 1 Dss-mediated Resolution Of Aβ In Alzheimer's Diseasementioning

confidence: 99%

Does Infection-Induced Immune Activation Contribute to Dementia?

Barichello¹,

Generoso²,

Goularte³

et al. 2015

Aging and disease

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Danggui-Shaoyao-San (DSS), also called Toki-shakuyaku-san (TJ-23) or Dangguijakyaksan (DJS), is a well-known herbal formula (Angelica sinensis (Oliv.) Diels., Ligusticum chuanxiong Hort., Paeonia lactiflora pall., Poria cocos (Schw.) Wolf, Alisma orientalis (Sam.) Juzep., Atractylodes macrocephala Koidz.), which has been widely used in oriental countries for the treatment of various gynecological diseases. Recent studies show that DSS has an effect on free radical-mediated neurological diseases and exhibits anti-inflammatory and antioxidant activities and reduces cell apoptosis in the hippocampus. In addition, DSS mediates the modulation of central monoamine neurotransmitter systems and ameliorates dysfunction of the central cholinergic nervous system and scopolamine-induced decrease in ACh levels. DSS improves the function of the dopaminergic, adrenergic, and serotonergic nervous systems. Interestingly, DSS can alleviate cognitive dysfunction of Alzheimer's disease (AD) patients, suggesting that it is a useful therapeutic agent for AD. This paper reviews the mechanism of DSS for the treatment of AD.

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Inhibition of β-Amyloid Aggregation by Albiflorin, Aloeemodin and Neohesperidin and their Neuroprotective Effect on Primary Hippocampal Cells Against β-Amyloid Induced Toxicity

Cited by 46 publications

References 17 publications

The neuroprotective effect of hesperidin in NMDA-induced retinal injury acts by suppressing oxidative stress and excessive calpain activation

The neuroprotective effect of hesperidin in NMDA-induced retinal injury acts by suppressing oxidative stress and excessive calpain activation

Emodin relieves hypoxia-triggered injury via elevation of microRNA-25 in PC-12 cells

Does Infection-Induced Immune Activation Contribute to Dementia?

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