• Title/Summary/Keyword: neurotoxicity

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Hypothetical Mechanisms of G protein-coupled neurodegeneration in glutamate excitotoxicity in human SH-SY5Y neuroblastoma cells

  • Nikolova, Nikolova Sevdalina;Jin, Da-Qing;Kim, Jung-Ae
    • Proceedings of the PSK Conference
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    • 2003.10b
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    • pp.123.2-123.2
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    • 2003

  • The cellular mechanisms by which excess exposure to the excitatory neurotransmitter glutamate can produce neuronal injury are unknown. In this study, we found that glutamate induced cell death at IC (50) of 100 microM on the cultured human SH-SY5Y neuroblastoma cells. It has been hypothesized that glutamate excitotoxicity is related with the elevation of calcium (Ca) levels. To determine the dependence of glutamate neurotoxicity on Ca environment, extracellular (EDTA) and intracellular (BAPTA/AM) chelator were used. (omitted)

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Effect of Ramulus et uncus uncariae on Glucose Oxidase-Induced Toxicity in Cultured Cerebral Neurons (조구등이 Glucose Oxidase로 손상된 대뇌신경세포에 미치는 효과)

  • Kim Hyeong Soo;Lee Yong Suk;Oh Suk Kyu;Lee Kang Chang;Lee Geon Mok;Lee Jeong;Lee Sang Bork;Kim Jong Ho;Yu Jun Ki;Kang Young Seong;Kim Sung Soo;Song Ho Jun;Park Seung Taeck
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.16 no.5
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    • pp.1016-1019
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    • 2002

  • To examine the cytotoxic effect of glucose oxidase(GO) in cultured mouse cerebral neurons, cytotoxicity was measured by MTT assay after cultured nerve cells were incubated for 3 hours in the media containing 1 ～ 60mU/ml concentrations of GO. In addition, the neuroprotective effect of Ramulus et uncus uncariae(REUU) was determined by MTT assay in these cultrures. Cell viability was remarkably decreased in a dose- and time-dependent manner after cultured mouse cerebral neurons were exposed to 30mU/ml GO for 3 hours. In the neuroprotective effect of REUU on GO-induced toxicity, REUU blocked the GO-mediated neurotoxicity in these cultures. From above the results, it suggests that GO is toxic in cultured mouse cerebral neurons and selective herb extract such as REUU is effective in prevetion of the neurotoxicity induced by GO.

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Protective Effect of Sanguisorba officinalis L. Root on Amyloid ${\beta}$ Protein (25-35)-induced Neuronal Cell Damage in Cultured Rat Cortical Neuron

  • Ban, Ju-Yeon;Cho, Soon-Ock;Jeon, So-Young;Song, Kyung-Sik;Bae, Ki-Hwan;Seong, Yeon-Hee
    • Korean Journal of Medicinal Crop Science
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    • v.13 no.5
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    • pp.219-226
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    • 2005

  • Sanguisorbae radix (SR) from Sanguisorba officinalis L. (Losaceae) is widely used in Korea and China due to its various pharmacological activity. The present study aims to investigate the effect of the methanol extract of SR on amyloid ${\beta}$ Protein(25-35) $(A{\beta}\;(25-35))$, a synthetic 25-35 amyloid peptide, -induced neurotoxicity using cultured rat cortical neurons. SR, over a concentration range of $10-50\;{\mu}g/ml$, inhibited the $A{\beta}$ (25-35) $(10\;{\mu}M)-induced$ neuronal cell death, as assessed by a 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and the number of apoptotic nuclei, evidenced by Hoechst 33342 staining. Pretreatment of SR $(50\;{\mu}g/ml)$ inhibited $10\;{\mu}M\;A{\beta}$ (25-35)-induced} elevation of cytosolic calcium concentration $([Ca^{2+}]c)$, which was measured by a fluorescent dye, fluo-4 AM. SR $(10\;and\;50\;{\mu}g/ml)$ inhibited glutamate release into medium induced by $10\;{\mu}M\;A{\beta}(25-35)$, which was measured by HPLC, and generation of reactive oxygen species. These results suggest that SR prevents $A{\beta}$ (25-35)-induced neuronal cell damage in vitro.

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