Neuroprotection against Aβ25–35-induced apoptosis by Salvia miltiorrhiza extract in SH-SY5Y cells

Hou, Yu; Yao, Lihua; Zhou, Huiping; Qu, Shen; Zeng, Xianghai; Zhou, Delong; Zhou, Yulian; Li, Xinglin; Liu, Zhicheng

doi:10.1016/j.neuint.2014.06.001

Cited by 53 publications

(42 citation statements)

References 46 publications

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“…Our previous study also showed that Aβ 25–35 could result in neuroinflammatory response and dysfunction of neurotrophin system [34]. As such, Aβ 25–35 has been popularly utilized to induce in vitro or in vivo AD models [32,33,35,36]. The present study demonstrates that 4-2A protects the SH-SY5Y cells from Aβ 25–35- induced reduction in cell viability by suppressing oxygen stress and inflammation, regulating neurotrophin levels, hence attenuating neuron apoptosis.…”

Section: Discussionmentioning

confidence: 99%

An Extract from Shrimp Processing By-Products Protects SH-SY5Y Cells from Neurotoxicity Induced by Aβ25–35

et al. 2017

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Increased evidence suggests that marine unsaturated fatty acids (FAs) can protect neurons from amyloid-β (Aβ)-induced neurodegeneration. Nuclear magnetic resonance (NMR), high performance liquid chromatography (HPLC) and gas chromatography (GC) assays showed that the acetone extract 4-2A obtained from shrimp Pandalus borealis industry processing wastes contained 67.19% monounsaturated FAs and 16.84% polyunsaturated FAs. The present study evaluated the anti-oxidative and anti-inflammatory effects of 4-2A in Aβ25–35-insulted differentiated SH-SY5Y cells. Cell viability and cytotoxicity were measured by using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays. Quantitative PCR and Western blotting were used to study the expression of neurotrophins, pro-inflammatory cytokines and apoptosis-related genes. Administration of 20 μM Aβ25–35 significantly reduced SH-SY5Y cell viability, the expression of nerve growth factor (NGF) and its tyrosine kinase TrkA receptor, as well as the level of glutathione, while increased reactive oxygen species (ROS), nitric oxide, tumor necrosis factor (TNF)-α, brain derived neurotrophic factor (BDNF) and its TrkB receptor. Aβ25–35 also increased the Bax/Bcl-2 ratio and Caspase-3 expression. Treatment with 4-2A significantly attenuated the Aβ25–35-induced changes in cell viability, ROS, GSH, NGF, TrkA, TNF-α, the Bax/Bcl-2 ratio and Caspase-3, except for nitric oxide, BDNF and TrKB. In conclusion, 4-2A effectively protected SH-SY5Y cells against Aβ-induced neuronal apoptosis/death by suppressing inflammation and oxidative stress and up-regulating NGF and TrKA expression.

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Section: Discussionmentioning

confidence: 99%

An Extract from Shrimp Processing By-Products Protects SH-SY5Y Cells from Neurotoxicity Induced by Aβ25–35

et al. 2017

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“…45 Aβ 25−35 , a synthetic peptide that possesses the same β-sheet structure and exhibits large fibrils, possesses most of the physical and biological properties of full length-Aβ 46 and is often used to study the neuroprotective effects of various compounds predicted to modulate Aβ toxicity in vitro. 47 The 3-(4,5-dimethylthiazol-2- Table 3.…”

Section: Journal Of Natural Productsmentioning

confidence: 99%

Natural β-Dihydroagarofuran-Type Sesquiterpenoids as Cognition-Enhancing and Neuroprotective Agents from Medicinal Plants of the Genus Celastrus

et al. 2015

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Alzheimer's disease (AD) is an irreversible, multifaceted, and progressive neurodegenerative disorder. Over the past 30 years, the search for anti-AD drugs has been primarily based on the cholinergic deficiency hypothesis and/or the β-amyloid (Aβ) cascade hypothesis. In this study, we report the identification of 16 new and 38 known β-dihydroagarofuran-type sesquiterpenoids from Celastrus flagellaris and Celastrus angulatus. The β-dihydroagarofuran-type sesquiterpenoids 58, 59, 61, and 63 significantly attenuated scopolamine-induced prolonged escape latency and increased number of errors compared with the control group. At 10 μM, 21 of the 62 tested β-dihydroagarofuran-type sesquiterpenoids rescued Aβ25-35-induced SH-SY5Y cells from viability reduction, which increased the cell viability from 64.6% for the model to more than 74.0%. The majority of the β-dihydroagarofuran-type sesquiterpenoids with ester groups exhibited stronger activity than those with free hydroxy groups or without substituents at the same positions. These results identified a new chemical skeleton as drug lead for the investigation of novel therapeutic agents against AD.

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“…SH‐SY5Y cells, established in 1970, were derived from a subgroup of metastatic neuroblastoma tumor cells, SK‐N‐SH, after three rounds of cloning (SK‐N‐SH → SH‐SY → SH‐SY5 → SH‐SY5Y; Biedler, Helson, & Spengler, ). These cells have been widely used as an in vitro model of neuronal function and differentiation in neurobiology research (Agholme, Lindström, Kågedal, Marcusson, & Hallbeck, ; Cañas et al, ; Yu et al, ). The applicability of SH‐SY5Y cell differentiation remains controversial (Goldie, Barnett, & Cairns, ); SH‐SY5Y cells are derived from humans and are differentiated from neurons, but they also exhibit cancer cell characteristics, such as their ability to divide continuously and are also used in neurobiology studies.…”

Section: Discussionmentioning

confidence: 99%

Genistein inhibits Aβ_25–35‐induced SH‐SY5Y cell damage by modulating the expression of apoptosis‐related proteins and Ca²⁺ influx through ionotropic glutamate receptors

Wang

et al. 2018

Phytotherapy Research

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In this study, we investigated the protective effects of genistein against SH-SY5Y cell damage induced by β-amyloid 25-35 peptide (Aβ 25-35 ) and the underlying mechanisms. Aβ-induced neuronal death, apoptosis, glutamate receptor subunit expression, Ca 2+ ion concentration, amino acid transmitter concentration, and apoptosis-related factor expression were evaluated to determine the effects of genistein on Aβ-induced neuronal death and apoptosis. The results showed that genistein increased the survival of SH-SY5Y cells and decreased the level of apoptosis induced by Aβ 25-35 . In addition, genistein reversed the Aβ 25-35 -induced changes in amino acid transmitters, α-amino-3hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors, and N-methyl-D-aspartate (NMDA) receptor subunits in SH-SY5Y cells. Aβ 25-35 -induced changes in Ca 2+ and Bcell lymphoma-2 (Bcl-2) and Bcl-2-associated X (Bax) protein and gene levels in cells were also reversed by genistein. Our data suggest that genistein protects against Aβ 25-35induced damage in SH-SY5Y cells, possibly by regulating the expression of apoptosis-related proteins and Ca 2+ influx through ionotropic glutamate receptors.

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Neuroprotection against Aβ25–35-induced apoptosis by Salvia miltiorrhiza extract in SH-SY5Y cells

Cited by 53 publications

References 46 publications

An Extract from Shrimp Processing By-Products Protects SH-SY5Y Cells from Neurotoxicity Induced by Aβ25–35

An Extract from Shrimp Processing By-Products Protects SH-SY5Y Cells from Neurotoxicity Induced by Aβ25–35

Natural β-Dihydroagarofuran-Type Sesquiterpenoids as Cognition-Enhancing and Neuroprotective Agents from Medicinal Plants of the Genus Celastrus

Genistein inhibits Aβ_25–35‐induced SH‐SY5Y cell damage by modulating the expression of apoptosis‐related proteins and Ca²⁺ influx through ionotropic glutamate receptors

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Neuroprotection against Aβ25–35-induced apoptosis by Salvia miltiorrhiza extract in SH-SY5Y cells

Cited by 53 publications

References 46 publications

An Extract from Shrimp Processing By-Products Protects SH-SY5Y Cells from Neurotoxicity Induced by Aβ25–35

An Extract from Shrimp Processing By-Products Protects SH-SY5Y Cells from Neurotoxicity Induced by Aβ25–35

Natural β-Dihydroagarofuran-Type Sesquiterpenoids as Cognition-Enhancing and Neuroprotective Agents from Medicinal Plants of the Genus Celastrus

Genistein inhibits Aβ25–35‐induced SH‐SY5Y cell damage by modulating the expression of apoptosis‐related proteins and Ca2+ influx through ionotropic glutamate receptors

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Genistein inhibits Aβ_25–35‐induced SH‐SY5Y cell damage by modulating the expression of apoptosis‐related proteins and Ca²⁺ influx through ionotropic glutamate receptors