Preventive effects of crocin on neuronal damages induced by D-galactose through AGEs and oxidative stress in human neuroblastoma cells (SH-SY5Y)

Heidari, Somaye; Mehri, Soghra; Shariaty, Vahidesadat; Hosseinzadeh, Hossein

doi:10.3831/kpi.2018.21.003

Cited by 16 publications

(5 citation statements)

References 38 publications

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“…Another research has clarified that Crocin can ameliorate memory deficiency by inhibiting Aβ‐induced apoptosis and oxidative stress (Asadi et al., 2015 ). Furthermore, Crocin has been reported to enhance the memory abilities of aging Wistar rats by exerting its antioxidant activities (Heidari et al., 2017 ). Although few studies definitively state whether Crocin can cross the blood‐brain barrier, several studies have demonstrated that Crocetin can cross the blood‐brain barrier (Shahbaz et al., 2022 ).…”

Section: Discussionmentioning

confidence: 99%

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Crocin ameliorates neuroinflammation and cognitive impairment in mice with Alzheimer's disease by activating PI3K/AKT pathway

Su,

Wang,

Shao

et al. 2024

Brain and Behavior

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BackgroundCrocin has a good prospect in the treatment of Alzheimer's disease (AD), but the mechanisms underlying its neuroprotective effects remain elusive. This study aimed to investigate the neuroprotective effects of Crocin and its underlying mechanisms in AD.MethodsAD mice were set up by injecting Aβ25‐35 solution into the hippocampus. Then, the AD mice were injected intraperitoneally with 40 mg/kg/day of Crocin for 14 days. Following the completion of Crocin treatment, an open‐field test, Y‐maze test and Morris water maze test were conducted to evaluate the impact of Crocin on spatial learning and memory deficiency in mice. The effects of Crocin on hippocampal neuron injury, proinflammatory cytokine expressions (IL‐1β, IL‐6, and TNF‐α), and PI3K/AKT signaling‐related protein expressions were measured using hematoxylin and eosin staining, Western blot, and quantitative real‐time polymerase chain reaction (qRT‐PCR) experiments, respectively.ResultsCrocin attenuated Aβ25‐35‐induced spatial learning and memory deficiency and hippocampal neuron injury. Furthermore, the Western blot and qRT‐PCR results showed that Crocin effectively suppressed inflammation and activated the PI3K/AKT pathway in Aβ25‐35‐induced mice.ConclusionCrocin restrained neuroinflammation via the activation of the PI3K/AKT pathway, thereby ameliorating the cognitive dysfunction of AD mice.

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Section: Discussionmentioning

confidence: 99%

“…For example, (Asadi et al, 2015). Furthermore, Crocin has been reported to enhance the memory abilities of aging Wistar rats by exerting its antioxidant activities (Heidari et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Crocin ameliorates neuroinflammation and cognitive impairment in mice with Alzheimer's disease by activating PI3K/AKT pathway

Su,

Wang,

Shao

et al. 2024

Brain and Behavior

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“…The cell cytotoxicity was measured using an MTT assay. The cells were seeded in a 96-well cell culture plate at a density of 1 × 10 4 cells per well for 24 h and then treated with Mel at different concentrations (0.1, 0.2, 0.4, 0.8, 1.0, 1.5, 2.0, 3.0, and 4.0 mg/ml) for 72 h. In another set of experiment, the cells were treated with DG (200 mM) [ 21 , 22 ] and Mel (1.5 mg/ml) separately and in combination for 72 h. To rule out the glucotoxicity, glucose (200 mM) treatment was also given in one group of cells. After completion of the treatment time, MTT (5 mg/ml) was added and incubated for a further 2 h at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Melamine Exacerbates Neurotoxicity in D-Galactose-Induced Neuronal SH-SY5Y Cells

Goyal,

Jain,

Jain

et al. 2023

Journal of Aging Research

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Numerous studies have depicted the role of diet and environmental toxins in aging. Melamine (Mel) is a globally known notorious food adulterant, and its toxicity has been shown in several organs including the brain. However, till now, there are no reports regarding Mel neurotoxicity in aging neurons. So, this study examined the in vitro neurotoxicity caused by Mel in the D-galactose (DG)-induced aging model of neuronal SH-SY5Y cells. In the present study, the neuronal SH-SY5Y cells were treated with DG and Mel separately and in combination to assess the neurotoxicity potential using MTT assay and neurite length measurement. Further, the superoxide dismutase (SOD), catalase (CAT), and total antioxidant activities were evaluated followed by the determination of the intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and caspase3 (Casp3) activity. The cotreatment of Mel and DG in neuronal SH-SY5Y cells showed maximum cell death than the cells treated with DG or Mel individually and untreated control cells. The neurite length shrinkage and ROS production were maximum in the DG and Mel cotreated cells showing exacerbated toxicity of Mel. The activity of SOD, CAT, and total antioxidants was also found to be lowered in the cotreatment group (Mel + DG) than in Mel- or DG-treated and untreated cells. Further, the combined toxicity of Mel and DG also elevated the Casp3 activity more than any other group. This is the first study showing the increased neurotoxic potential of Mel in an aging model of neuronal SH-SY5Y cells which implicates that Mel consumption by the elderly may lead to increased incidences of neurodegeneration like Alzheimer’s disease and Parkinson’s disease.

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“…Notably, only few studies have assessed the potential protective effect of Crocus sativus extracts and individual compounds against oxidative stress using neuronal cells, despite the significant antioxidant properties of crocins that are observed in animal and cellular models of neurodegenerative disorders (34,35). Previous studies employing neuronal retinal ganglion cells or proliferating SH-SY5Y cells reported a protective effect of low crocin concentrations (0.1-1 μM) against H2O2-induced toxicity (36), or other types of oxidative stress (36,37).…”

Section: Antioxidant and Neuroprotective Properties Of Crocus Sativus...mentioning

confidence: 99%

Crocus sativus, Olea Europea and Salvia spp: Role in Neuroprotection against H2O2 and Aβ-peptide Induced Cell Toxicity

Kofinas,

Pavlidis,

Andriopoulou

et al. 2023

Preprint

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Neurotoxicity belongs to the leading factors inducing neurodegeneration-related diseases, such as Alzheimer’s (AD) and Parkinson’s disease. In particular, accumulation of β-amyloid proteins in the brain, a hallmark in AD, induces oxidative stress and neurotoxicity. The use of antioxidants in AD is not sufficiently effective and other pharmacological approaches tested failed to cure, prevent or retard the progression of the disease. Clinical studies indicated that several medicinal plants display beneficial effects by improving memory and cognitive functions of patients with mild and moderate AD. In this study, the potential antioxidant and neuroprotective properties of Olea europea, Crocus sativus and Salvia spp extracts, as well as their main active compounds on cell viability was evaluated using an in vitro model of AD, the differentiated human SH-SY5Y neuroblastoma cells to cholinergic neurons. Their effects were assessed against the H2O2- and β-amyloid- induced cell toxicity using the MTS test. Current findings indicated that Salvia fruticosa, S. officinalis, S. argentea leaf extracts and the active compounds, oleuropein, trans-crocin-3 and -4 display significant dose-dependent antioxidant and neuroprotective properties. It is of note though that the total phenolic fragment of Olea europea leaf extract includes several toxic compounds, such as oleocanthal, that markedly reduce cell viability and exacerbate the H2O2- and Aβ-induced cell toxicity. In addition, the Crocus sativus hydrophilic and diethyl ether extracts and all their active compounds tested markedly increased the H2O2-induced cell toxicity. In conclusion, the medicinal plants tested contain several compounds displaying dose-dependent effects against H2O2- and Aβ-induced neurotoxicity and could be used in AD, but they also contain several neurotoxic agents.

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Preventive effects of crocin on neuronal damages induced by D-galactose through AGEs and oxidative stress in human neuroblastoma cells (SH-SY5Y)

Cited by 16 publications

References 38 publications

Crocin ameliorates neuroinflammation and cognitive impairment in mice with Alzheimer's disease by activating PI3K/AKT pathway

Crocin ameliorates neuroinflammation and cognitive impairment in mice with Alzheimer's disease by activating PI3K/AKT pathway

Melamine Exacerbates Neurotoxicity in D-Galactose-Induced Neuronal SH-SY5Y Cells

<em>Crocus sativus</em>, <em>Olea Europea</em> and <em>Salvia spp</em>: Role in Neuroprotection against H<sub>2</sub>O<sub>2</sub> and Aβ-peptide Induced Cell Toxicity

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