Neuroprotective effect of &amp;beta;-asarone against Alzheimer&amp;rsquo;s disease: regulation of synaptic plasticity by increased expression of SYP and GluR1

Liu, Sijun; Yang, Cong; Zhang, Yue; Su, Ruyu; Chen, Junli; Jiao, Mengmeng; Chen, Huifang; Zheng, Na; Luo, Si; Chen, Yunbo; Quan, Shijian; Wang, Qi

doi:10.2147/dddt.s93559

Cited by 53 publications

(50 citation statements)

References 35 publications

(27 reference statements)

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“…β-asarone is an ether found, e.g., in Acori graminei ( Liu et al, 2016 ). β-asarone treatment decreases Aβ42 levels in hippocampus and improves memory in a mouse model of AD, probably through mTOR-dependent autophagy ( Deng et al, 2016 ).…”

Section: Therapeutic Implications Of the Interplay Of Alzheimer’s Dismentioning

confidence: 99%

Autophagy and Alzheimer’s Disease: From Molecular Mechanisms to Therapeutic Implications

Uddin

Stachowiak

Mamun

et al. 2018

Front. Aging Neurosci.

317

247

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Alzheimer’s disease (AD) is the most common cause of progressive dementia in the elderly. It is characterized by a progressive and irreversible loss of cognitive abilities and formation of senile plaques, composed mainly of amyloid β (Aβ), and neurofibrillary tangles (NFTs), composed of tau protein, in the hippocampus and cortex of afflicted humans. In brains of AD patients the metabolism of Aβ is dysregulated, which leads to the accumulation and aggregation of Aβ. Metabolism of Aβ and tau proteins is crucially influenced by autophagy. Autophagy is a lysosome-dependent, homeostatic process, in which organelles and proteins are degraded and recycled into energy. Thus, dysfunction of autophagy is suggested to lead to the accretion of noxious proteins in the AD brain. In the present review, we describe the process of autophagy and its importance in AD. Additionally, we discuss mechanisms and genes linking autophagy and AD, i.e., the mTOR pathway, neuroinflammation, endocannabinoid system, ATG7, BCL2, BECN1, CDK5, CLU, CTSD, FOXO1, GFAP, ITPR1, MAPT, PSEN1, SNCA, UBQLN1, and UCHL1. We also present pharmacological agents acting via modulation of autophagy that may show promise in AD therapy. This review updates our knowledge on autophagy mechanisms proposing novel therapeutic targets for the treatment of AD.

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Section: Therapeutic Implications Of the Interplay Of Alzheimer’s Dismentioning

confidence: 99%

Autophagy and Alzheimer’s Disease: From Molecular Mechanisms to Therapeutic Implications

Uddin

Stachowiak

Mamun

et al. 2018

Front. Aging Neurosci.

317

247

View full text Add to dashboard Cite

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“…In the clinical context, β‐asarone exhibits various medicinal properties, such as anticancer (Liu et al, ; Wu et al, ; Zou et al, ), anti‐inflammatory, neuroprotective (Muthuraman & Singh, ), antiepileptic (Fu, Fang, Fang, Xie, & Fang, ), and antioxidant (Chaubey, Parki, Prakash, Kumar, & Pan, ) activities. β‐Asarone increased the expression of synaptophysin and glutamatergic receptor 1, deficiencies of which are associated with Alzheimer's disease, in APP/PS1 mice (Liu et al, ), and a 100‐mg/kg daily dose of β‐asarone improved learning and memory in a rat model of Alzheimer's disease because of galactose and aluminium chloride (Querfurth & LaFerla, ; Yan, Chen, Yan, Guo, & Chen, ).…”

Section: Introductionmentioning

confidence: 99%

Cytotoxic effects of β‐asarone on Sf9 insect cells

Yooboon

Kuramitsu

Bullangpoti

et al. 2019

Arch Insect Biochem Physiol

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β-Asarone is the predominant component of the essential oil of rhizomes of Acorus calamus Linn ( Sweet flag). Although rhizome extracts from this plant have long been used for insect pest control, their cytotoxic effects on insect cells are not well understood. In this study, we evaluated the potency of β-asarone as a natural insecticide by using a Spodoptera frugiperda cell line (Sf9). To assess the cytotoxic effects of β-asarone on Sf9 cells, we observed morphologic changes in treated cells and performed a cell proliferation assay and a DNA fragmentation assay. After 24 and 48 h of treatment with β-asarone, the proliferation of the Sf9 cells was inhibited in a dose-dependent manner, with IC 50 values of 0.558 mg/ml at 24 h and 0.253 mg/ml at 48 h. Morphologic changes in β-asarone-treated cells were typical of apoptosis and included loss of adhesion, cell shrinkage, and small apoptotic bodies. The DNA laddering present in β-asarone-treated SF9 cells and annexin V assay confirmed that this compound can induce apoptosis in insect cells.Together, these findings suggest that apoptosis induction may be one mechanism through which β-asarone inhibits the proliferation of insect cells and thus exerts insecticidal effects. K E Y W O R D S apoptosis, botanical pesticide, cell toxicity, Sf9, β-asarone

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“…In the present study, it was found that Bdnf and Gdnf gene expression was notably inhibited in HT22 cells cultured with HG, while fisetin pretreatment dramatically upregulated Bdnf and Gdnf expression, even higher than control group. Besides, it is widely believed that SYP can mediate synaptic structure and play a part in synaptic plasticity through phosphorylation and release of neurotransmitters (Liu et al, 2016). Chronic fluoride exposures reduced SYP expression and induced aberrant changes of GSK-3β/β-catenin signaling, leading to neuronal apoptosis and impaired synaptic plasticity (Jiang et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Fisetin Prevents HT22 Cells From High Glucose-Induced Neurotoxicity via PI3K/Akt/CREB Signaling Pathway

et al. 2020

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Hyperglycemia has been widely considered as a key risk factor for diabetic encephalopathy which can cause neuronal apoptosis and cognitive deficits. The flavonoid compound, fisetin, possesses potential neuroprotective effects and also enhances learning and memory. However, the role of fisetin in hyperglycemia-induced neuronal cytotoxicity has not been fully elucidated. In the present study, HT22 murine hippocampal neuronal cell line was used to establish the injured cell model. Cell proliferation and cytotoxicity assay, Hoechst 33258 staining, qRT-PCR, western blot analysis, and specific inhibitor were used to investigate the effect and molecular mechanisms of fisetin on high glucose (HG)-induced neurotoxicity in HT22 cells. Our results showed that 125 µM and 48 h of treatment was identified as optimal damage parameter of HG. Fisetin significantly improved HG-inhibited cell viability. The levels of LDH, malondialdehyde (MDA), and superoxide dismutase (SOD) were noticeably modulated by fisetin, which alleviated HG-induced HT22 cell oxidative damage. Besides, the apoptosis of HT22 cells was rescued by fisetin pretreatment. In addition, fisetin also prevented HG-induced downregulation of the mRNA expression of Bdnf, Gdnf, synaptophysin (Syp), and glutamate ionotropic receptor AMPA type subunit 1 (Gria1) in cells. More importantly, the decreased phosphorylation of phosphoinositide 3 kinase (PI3K), Akt, and cAMP-response element binding protein (CREB) was rescued by fisetin treatment and that neuroprotective effect of fisetin was partially blocked by PI3K inhibitor, LY294002. These findings indicate that fisetin has potent neuroprotective effect and prevents HG-induced neurotoxicity by activation of PI3K/Akt/CREB pathway.

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Neuroprotective effect of β-asarone against Alzheimer’s disease: regulation of synaptic plasticity by increased expression of SYP and GluR1

Cited by 53 publications

References 35 publications

Autophagy and Alzheimer’s Disease: From Molecular Mechanisms to Therapeutic Implications

Autophagy and Alzheimer’s Disease: From Molecular Mechanisms to Therapeutic Implications

Cytotoxic effects of β‐asarone on Sf9 insect cells

Fisetin Prevents HT22 Cells From High Glucose-Induced Neurotoxicity via PI3K/Akt/CREB Signaling Pathway

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