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p-Terphenyl curtisians protect cultured neuronal cells against glutamate neurotoxicity via iron chelation.
Planta Med. 2003 Jun; 69(6):513-7.PM

Abstract

The hyperactivity of ionotropic glutamate receptors has been implicated in the development of the neuronal cell death seen in many neurodegenerative processes including ischemic stroke, traumatic brain injury, and epilepsy. Thus neuronal protection against glutamate-induced neurotoxicity is considered as an appropriate therapeutic strategy for preventing and treating neurodegenerative diseases. Whilst searching for blockers of glutamate-induced toxicity in mouse cortical cells, we isolated p-terphenyl curtisians A - D from the mushroom Paxillus curtisii. Curtisians protected cortical neurons from glutamate-induced toxicity in a dose-dependent manner. Among the glutamate receptor subtypes, curtisians were found to block NMDA receptor-mediated but not AMPA/kainate-mediated cell death. In addition, we found that curtisians exhibited potent antioxidative activity against iron-mediated oxidative damage which was generated by H2O2 neurotoxocity and lipid peroxidation, but no activity was detected in the superoxide, DPPH and ABTS radical scavenging systems, and in protection of N18-RE-105 cells subjected to glutamate-induced glutathione depletion. This effect was likely due to the iron chelating properties of curtisians. The iron chelation ability of curtisians was then further investigated on DNA single strand breakage (SSB) induced by the addition of iron and H2O2, and curtisians prevented DNA SSB like the iron chelator desferrioxamine. These results suggest that the neuroprotective action of curtisians is dependent on their ability to chelate iron as well as to block the NMDA receptor, and that in this context curtisians may be useful as neuroprotective agents against neurological disorders which result in neuronal cell death.

Authors+Show Affiliations

Laboratory of Antioxidant, Korea Research Institute of Bioscience and Biotechnology, Yusong, Daejon, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12865968

Citation

Lee, In-Kyoung, et al. "P-Terphenyl Curtisians Protect Cultured Neuronal Cells Against Glutamate Neurotoxicity Via Iron Chelation." Planta Medica, vol. 69, no. 6, 2003, pp. 513-7.
Lee IK, Yun BS, Kim JP, et al. P-Terphenyl curtisians protect cultured neuronal cells against glutamate neurotoxicity via iron chelation. Planta Med. 2003;69(6):513-7.
Lee, I. K., Yun, B. S., Kim, J. P., Kim, W. G., Ryoo, I. J., Oh, S., Kim, Y. H., & Yoo, I. D. (2003). P-Terphenyl curtisians protect cultured neuronal cells against glutamate neurotoxicity via iron chelation. Planta Medica, 69(6), 513-7.
Lee IK, et al. P-Terphenyl Curtisians Protect Cultured Neuronal Cells Against Glutamate Neurotoxicity Via Iron Chelation. Planta Med. 2003;69(6):513-7. PubMed PMID: 12865968.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - p-Terphenyl curtisians protect cultured neuronal cells against glutamate neurotoxicity via iron chelation. AU - Lee,In-Kyoung, AU - Yun,Bong-Sik, AU - Kim,Jong-Pyung, AU - Kim,Won-Gon, AU - Ryoo,In-Ja, AU - Oh,Seikwan, AU - Kim,Young-Ho, AU - Yoo,Ick-Dong, PY - 2003/7/17/pubmed PY - 2003/10/22/medline PY - 2003/7/17/entrez SP - 513 EP - 7 JF - Planta medica JO - Planta Med VL - 69 IS - 6 N2 - The hyperactivity of ionotropic glutamate receptors has been implicated in the development of the neuronal cell death seen in many neurodegenerative processes including ischemic stroke, traumatic brain injury, and epilepsy. Thus neuronal protection against glutamate-induced neurotoxicity is considered as an appropriate therapeutic strategy for preventing and treating neurodegenerative diseases. Whilst searching for blockers of glutamate-induced toxicity in mouse cortical cells, we isolated p-terphenyl curtisians A - D from the mushroom Paxillus curtisii. Curtisians protected cortical neurons from glutamate-induced toxicity in a dose-dependent manner. Among the glutamate receptor subtypes, curtisians were found to block NMDA receptor-mediated but not AMPA/kainate-mediated cell death. In addition, we found that curtisians exhibited potent antioxidative activity against iron-mediated oxidative damage which was generated by H2O2 neurotoxocity and lipid peroxidation, but no activity was detected in the superoxide, DPPH and ABTS radical scavenging systems, and in protection of N18-RE-105 cells subjected to glutamate-induced glutathione depletion. This effect was likely due to the iron chelating properties of curtisians. The iron chelation ability of curtisians was then further investigated on DNA single strand breakage (SSB) induced by the addition of iron and H2O2, and curtisians prevented DNA SSB like the iron chelator desferrioxamine. These results suggest that the neuroprotective action of curtisians is dependent on their ability to chelate iron as well as to block the NMDA receptor, and that in this context curtisians may be useful as neuroprotective agents against neurological disorders which result in neuronal cell death. SN - 0032-0943 UR - https://www.unboundmedicine.com/medline/citation/12865968/p_Terphenyl_curtisians_protect_cultured_neuronal_cells_against_glutamate_neurotoxicity_via_iron_chelation_ L2 - http://www.thieme-connect.com/DOI/DOI?10.1055/s-2003-40650 DB - PRIME DP - Unbound Medicine ER -