Neuroprotective effects of constituents of the root bark of Dictamnus dasycarpus in mouse hippocampal cells

Jeong, Gil‐Saeng; Byun, Erisa; Li, Bin; Lee, Dong-Sung; Kim, Youn‐Chul; An, Ru

doi:10.1007/s12272-010-0818-9

Cited by 47 publications

(30 citation statements)

References 30 publications

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“…Although it is the main excitatory neurotransmitter in neurons, excessive accumulation of glutamate can not only activate ROS production and oxidative neurotoxicity contributing to neuronal apoptosis [1,6], but associate with acute and chronic NDs as well [7,8]. Multiple lines of evidence have supported that glutamate-induced apoptosis relates to the cysteine uptake through the cysteine/glutamate antiporter channel, leading to the diminution of endogenous antioxidant glutathione and increase of ROS in neurons [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Cyanidin-3-glucoside activates Nrf2-antioxidant response element and protects against glutamate-induced oxidative and endoplasmic reticulum stress in HT22 hippocampal neuronal cells

Sukprasansap

Chanvorachote

Tencomnao

2020

BMC Complement Med Ther

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Background: Cyanidin-3-glucoside (C3G), a major anthocyanin present in berries, exhibits a strong antioxidant and has been shown to possess a neuroprotection. Prolonged exposure to glutamate will lead to oxidative damage and endoplasmic reticulum stress which could play a key detrimental role in the development of neurodegenerative disorders (NDs). In the present study, we investigated the neuroprotective effect and underlying mechanisms of C3G on the reduction of oxidative/ER stress-induced apoptosis by glutamate in HT22 mouse hippocampal neuronal cells.Method: Cells were pre-treated with C3G in various concentrations, followed by glutamate. Cell viability and toxicity were examined using MTT and LDH assays. The apoptotic and necrotic cell death were carried out by Annexin V-FITC/propidium iodide co-staining assays. Generation of intracellular reactive oxygen species (ROS) in cells was measured by flow cytometry using DCFH-DA probe. Expression of antioxidant genes was evaluated by Real-time polymerase chain reaction analysis. The possible signaling pathways and proteins involved were subsequently demonstrated by Western blot analysis.Result: The pretreatment of the HT22 cells with C3G protected cell death from oxidative toxicity induced by glutamate. We demonstrated that treatment cells with glutamate caused several radical forms of ROS formation, and they were abolished by specific ROS inhibitors. Interestingly, C3G directly scavenged radical activity and inhibited intracellular ROS generation in our cell-based system. In addition, C3G pretreatment suppressed the up-regulation of specific ER proteins namely calpain, caspase-12 and C/EBP homologous proteins (CHOP) induced by glutamate-mediated oxidative and ER stress signal by upregulating the expressions of survival proteins, including extracellular regulated protein kinase (ERK) and nuclear factor E2related factor 2 (Nrf2). Furthermore, dramatically activated gene expression of endogenous antioxidant enzymes (i.e. superoxide dismutases (SODs), catalase (CAT) and glutathione peroxidase (GPx)), and phase II enzymes (glutathione-Stransferases (GSTs)) was found in C3G-treated with cells.Conclusions: Our finding suggest that C3G could be a promising neuroprotectant via inhibition of glutamate-induced oxidative and ER stress signal and activation of ERK/Nrf2 antioxidant mechanism pathways.

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Section: Introductionmentioning

confidence: 99%

Cyanidin-3-glucoside activates Nrf2-antioxidant response element and protects against glutamate-induced oxidative and endoplasmic reticulum stress in HT22 hippocampal neuronal cells

Sukprasansap

Chanvorachote

Tencomnao

2020

BMC Complement Med Ther

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“…4 Limonoids exhibited a wide spectrum of biological properties including cytotoxic, [5][6][7][8] antioxidant, 9,10 antiinammatory, 11,12 neuroprotective, 13,14 antiviral, 15 antimicrobial, 16,17 antiprotozoal, 18 antimalarial, [19][20][21] insect antifeedant, [22][23][24][25][26] and insecticidal activities. [27][28][29] The present review highlights the advances of limonoids in regard to isolation, total synthesis, and structural modications with the relevant biological properties.…”

Section: Introductionmentioning

confidence: 99%

Recent progress in the chemistry and biology of limonoids

Zhang

2017

RSC Adv.

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“…It was found that the immortalized hippocampus-derived HT22 cells, which had the characteristics of lacking the functional ionotropic glutamate receptor (Jeong et al 2010), were considered as a very useful cell model for investigating oxidative glutamate impairment excluding glutamate receptor-mediated excitotoxicity.…”

Section: Introductionmentioning

confidence: 99%

Huperzine A Alleviates Oxidative Glutamate Toxicity in Hippocampal HT22 Cells via Activating BDNF/TrkB-Dependent PI3K/Akt/mTOR Signaling Pathway

Mao

Zhou

et al. 2015

Cell Mol Neurobiol

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Oxidative glutamate toxicity is involved in diverse neurological disorders including epilepsy and ischemic stroke. Our present work aimed to assess protective effects of huperzine A (HupA) against oxidative glutamate toxicity in a mouse-derived hippocampal HT22 cells and explore its potential mechanisms. Cell survival and cell injury were analyzed by MTT method and LDH release assay, respectively. The production of ROS was measured by detection kits. Protein expressions of BDNF, phosphor-TrkB (p-TrkB), TrkB, phosphor-Akt (p-Akt), Akt, phosphor-mTOR (p-mTOR), mTOR, phosphor-p70s6 (p-p70s6) kinase, p70s6 kinase, Bcl-2, Bax, and β-actin were assayed via Western blot analysis. Enzyme-linked immunosorbent assay was employed to measure the contents of nerve growth factor, brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4). Our findings illustrated 10 μM HupA for 24 h significantly protected HT22 from cellular damage and suppressed the generation of ROS. Additionally, after treating with LY294002 or wortmannin [the selective inhibitors of phosphatidylinositol 3 kinase (PI3K)], HupA dramatically prevented the down-regulations of p-Akt, p-mTOR, and p-p70s6 kinase in HT22 cells under oxidative toxicity. Furthermore, it was observed that the protein levels of BDNF and p-TrkB were evidently enhanced after co-treatment with HupA and glutamate in HT22 cells. The elevations of p-Akt and p-mTOR were abrogated under toxic conditions after blockade of TrkB by TrkB IgG. Cellular apoptosis was significantly suppressed (decreased caspase-3 activity and enhanced Bcl-2 protein level) after HupA treatment. It was concluded that HupA attenuated oxidative glutamate toxicity in murine hippocampal HT22 cells via activating BDNF/TrkB-dependent PI3K/Akt/mTOR signaling pathway.

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Neuroprotective effects of constituents of the root bark of Dictamnus dasycarpus in mouse hippocampal cells

Cited by 47 publications

References 30 publications

Cyanidin-3-glucoside activates Nrf2-antioxidant response element and protects against glutamate-induced oxidative and endoplasmic reticulum stress in HT22 hippocampal neuronal cells

Cyanidin-3-glucoside activates Nrf2-antioxidant response element and protects against glutamate-induced oxidative and endoplasmic reticulum stress in HT22 hippocampal neuronal cells

Recent progress in the chemistry and biology of limonoids

Huperzine A Alleviates Oxidative Glutamate Toxicity in Hippocampal HT22 Cells via Activating BDNF/TrkB-Dependent PI3K/Akt/mTOR Signaling Pathway

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