Low concentrations of 1-methyl-4-phenylpyridinium ion induce caspase-mediated apoptosis in human SH-SY5Y neuroblastoma cells

Gómez, Cristina; Reiriz, Julia; Piqué, Maria; Gil, Joan; Ferrer, Isidre; Ambrosio, Santiago

doi:10.1002/1097-4547(20010301)63:5<421::aid-jnr1037>3.0.co;2-4

Cited by 64 publications

(52 citation statements)

References 53 publications

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“…Neuroprotection against Ab b 25-35 -Induced Neuronal Death in Hippocampal Neurons Since these tetrahydrofuran-type neolignans (1-7) showed promising neurotrophic effects in cultured rat cortical neurons, we further investigated their neuroprotective effects against Ab [25][26][27][28][29][30][31][32][33][34][35] inducedneuronal death in primary cultured rat hippocampal neurons. In our preliminary experiment, Ab [25][26][27][28][29][30][31][32][33][34][35] dose dependently induced cell death in cultured hippocampal neurons at concentrations higher than 5 mM (data not shown).…”

Section: Neurotrophic Effects In Cultured Cortical Neuronsmentioning

confidence: 99%

“…In our preliminary experiment, Ab [25][26][27][28][29][30][31][32][33][34][35] dose dependently induced cell death in cultured hippocampal neurons at concentrations higher than 5 mM (data not shown). The morphology of hippocampal neurons cultured for 72 h showed indications of good viability, including healthy soma and long neurites (Fig.…”

Section: Neurotrophic Effects In Cultured Cortical Neuronsmentioning

confidence: 99%

“…The morphology of hippocampal neurons cultured for 72 h showed indications of good viability, including healthy soma and long neurites (Fig. 4A) After Ab [25][26][27][28][29][30][31][32][33][34][35] exposure for 48 h, many dead neurons appeared in each field when observed under a microscope; neuritic processes became shortened, damaged, or disappeared (Fig. 4B).…”

Section: Neurotrophic Effects In Cultured Cortical Neuronsmentioning

confidence: 99%

“…1) from a methanol extract of the same plant. In this paper, we report the neurotrophic effects of these 2,5-diaryl-3,4-dimethyltetrahydrofuran neolignans (2-7) for comparison with 1, the neuroprotective effects of neolignans (1-7) against Ab [25][26][27][28][29][30][31][32][33][34][35] -induced cell death in primary cultured rat hippocampal neurons, 15) as well as against cell death induced by 1-methyl-4-phenylpyridinium ion (MPP ϩ ), a neurotoxin used in the cellular model for Parkinson's disease. 16) 17) and its analogues, veraguensin (2), 18) galgravin (3), 19) aristolignin (4), 19) nectandrin A (5), 20) isonectandrin B (6), 20) and nectandrin B (7), 20) were isolated from a methanol extract of the root of A. arcuata as previously described.…”

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confidence: 99%

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Neuroprotective Effects of 2,5-Diaryl-3,4-dimethyltetrahydrofuran Neolignans

Zhai

Inoue

Moriyama

et al. 2005

Biological & Pharmaceutical Bulletin

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We previously reported the neurotrophic effects of talaumidin (1) from Aristolochia arcuata MASTERS. In the present study, we compared the neurotrophic and neuroprotective effects of six other 2,5-diaryl-3,4-dimethyltetrahydrofuran neolignans isolated from the same plant, veraguensin (2), galgravin (3), aristolignin (4), nectandrin A (5), isonectandrin B (6), and nectandrin B (7), with compound 1 in primary cultured rat neurons. Compounds 3-7 promoted neuronal survival and neurite outgrowth, among which compounds 6 and 7 showed neurotrophic activity comparable with that of 1.

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Section: Neurotrophic Effects In Cultured Cortical Neuronsmentioning

confidence: 99%

Section: Neurotrophic Effects In Cultured Cortical Neuronsmentioning

confidence: 99%

Section: Neurotrophic Effects In Cultured Cortical Neuronsmentioning

confidence: 99%

mentioning

confidence: 99%

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Neuroprotective Effects of 2,5-Diaryl-3,4-dimethyltetrahydrofuran Neolignans

Zhai

Inoue

Moriyama

et al. 2005

Biological & Pharmaceutical Bulletin

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“…We calculated the ratio between fluorescence intensity at 590 and 530 nm for each well and expressed the ratio in treated samples as a percentage control, as previously described. 62 Each individual treatment/time point reflects four replicates.…”

Section: Measurement Of Mitochondrial Membrane Potential (Dw M )mentioning

confidence: 99%

Anandamide-induced cell death in primary neuronal cultures: role of calpain and caspase pathways

et al. 2004

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Anandamide (arachidonoylethanolamide or AEA) is an endocannabinoid that acts at vanilloid (VR1) as well as at cannabinoid (CB1/CB2) and NMDA receptors. Here, we show that AEA, in a dose-dependent manner, causes cell death in cultured rat cortical neurons and cerebellar granule cells. Inhibition of CB1, CB2, VR1 or NMDA receptors by selective antagonists did not reduce AEA neurotoxicity. Anandamideinduced neuronal cell loss was associated with increased intracellular Ca 2 þ , nuclear condensation and fragmentation, decreases in mitochondrial membrane potential, translocation of cytochrome c, and upregulation of caspase-3-like activity. However, caspase-3, caspase-8 or caspase-9 inhibitors, or blockade of protein synthesis by cycloheximide did not alter anandamide-related cell death. Moreover, AEA caused cell death in caspase-3-deficient MCF-7 cell line and showed similar cytotoxic effects in caspase-9 dominantnegative, caspase-8 dominant-negative or mock-transfected SH-SY5Y neuroblastoma cells. Anandamide upregulated calpain activity in cortical neurons, as revealed by a-spectrin cleavage, which was attenuated by the calpain inhibitor calpastatin. Calpain inhibition significantly limited anandamide-induced neuronal loss and associated cytochrome c release. These data indicate that AEA neurotoxicity appears not to be mediated by CB1, CB2, VR1 or NMDA receptors and suggest that calpain activation, rather than intrinsic or extrinsic caspase pathways, may play a critical role in anandamide-induced cell death.

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Parkinson Disease ‐Targeted Nanocapsules for Synergistic Treatment: Combining Dopamine Replacement and Neuroinflammation Mitigation

Liu,

Xiang,

Chen

et al. 2024

Advanced Science

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Parkinson's disease (PD) is characterized by dopamine (DA) neuron loss and neuroinflammation. This study develops carrier‐free nanocapsules (NCs) for targeted delivery of DA and catalase (CAT) to the PD brain, addressing both DA depletion and neuroinflammation simultaneously. The NCs are engineered by DA and 4‐formylphenylboronic acid co‐loading with cRGD‐modified CAT (CAT‐cRGD) and surface‐modifying with Angiopep‐2 (Ang). Ang targets the blood‐brain barrier (BBB), enhancing brain delivery, while cRGD targets upregulated integrin receptors in the PD‐affected BBB. The NCs showed a 1.4‐fold increase in parkinsonian brain targeting efficiency compared to normal mice. In PD mice models, NCs demonstrated a stable increase in learning and memory, enhanced locomotor activity, and improved motor coordination. DA supplementation significantly enhanced dopaminergic signaling, increasing DA levels 1.8‐ and 3.5‐fold in the striatum and substantia nigra, respectively. Additionally, delivered CAT effectively reduced neuroinflammation by mitigating endoplasmic reticulum stress, slowing disease progression, and protecting DA from oxidation. This innovative approach using PD‐targeted NCs represents a synergistic strategy for PD treatment, combining symptomatic relief with disease progression intervention.

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Low concentrations of 1-methyl-4-phenylpyridinium ion induce caspase-mediated apoptosis in human SH-SY5Y neuroblastoma cells

Cited by 64 publications

References 53 publications

Neuroprotective Effects of 2,5-Diaryl-3,4-dimethyltetrahydrofuran Neolignans

Neuroprotective Effects of 2,5-Diaryl-3,4-dimethyltetrahydrofuran Neolignans

Anandamide-induced cell death in primary neuronal cultures: role of calpain and caspase pathways

Parkinson Disease ‐Targeted Nanocapsules for Synergistic Treatment: Combining Dopamine Replacement and Neuroinflammation Mitigation

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