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Decursinol and decursin protect primary cultured rat cortical cells from glutamate-induced neurotoxicity.
J Pharm Pharmacol. 2007 Jun; 59(6):863-70.JP

Abstract

We previously reported six neuroprotective decursinol derivatives, coumarins from Angelica gigas (Umbelliferae) roots. To elucidate the action patterns of decursinol derivatives, we investigated the neuroprotective effects of decursinol and decursin, which showed highly significant activity and were major constituents of A. gigas, using primary cultures of rat cortical cells in-vitro. At concentrations of 0.1-10.0 microM, both decursinol and decursin exerted a significant neuroprotective activity pretreatment and throughout treatment. In addition, decursin had a neuroprotective impact in the post-treatment paradigm implying that decursin might possess different action mechanisms from that of decursinol in the protection of neurons against glutamate injury. Both decursinol and decursin effectively reduced the glutamate-induced increased intracellular calcium ([Ca(2+)](i)) in cortical cells, suggesting that these two coumarins may exert neuroprotection by reducing calcium influx by overactivation of glutamate receptors. This suggestion was supported by the result that decursinol and decursin protected neurons against kainic acid (KA)-induced neurotoxicity better than against that induced by N-methyl-D-aspartate (NMDA). Moreover, both decursinol and decursin significantly prevented glutamate-induced decreases in glutathione, a cellular antioxidant, and glutathione peroxidase activity. In addition, both compounds efficiently reduced the overproduction of cellular peroxide in glutamate-injured cortical cells. These results suggested that both decursinol and decursin protected primary cultured rat cortical cells against glutamate-induced oxidative stress by both reducing calcium influx and acting on the cellular antioxidative defence system. Moreover, decursin is considered to probably have a different action mechanism from that of decursinol in protecting cortical cells against glutamate injury.

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Authors+Show Affiliations

Kang SY
College of Pharmacy and Research Institute of Pharmaceutical Science, Seoul National University, Seoul 151-742, Republic of Korea.
Kim YC
No affiliation info available

MeSH

AngelicaAnimalsAntioxidantsBenzopyransButyratesCells, CulturedCerebral CortexGlutamic AcidGlutathioneGlutathione PeroxidaseKainic AcidN-MethylaspartateNeuronsNeuroprotective AgentsOxidative StressRatsRats, Sprague-Dawley

Pub Type(s)

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

Language

eng

PubMed ID

17637179

Citation

Kang, So Young, and Young Choong Kim. "Decursinol and Decursin Protect Primary Cultured Rat Cortical Cells From Glutamate-induced Neurotoxicity." The Journal of Pharmacy and Pharmacology, vol. 59, no. 6, 2007, pp. 863-70.
Kang SY, Kim YC. Decursinol and decursin protect primary cultured rat cortical cells from glutamate-induced neurotoxicity. J Pharm Pharmacol. 2007;59(6):863-70.
Kang, S. Y., & Kim, Y. C. (2007). Decursinol and decursin protect primary cultured rat cortical cells from glutamate-induced neurotoxicity. The Journal of Pharmacy and Pharmacology, 59(6), 863-70.
Kang SY, Kim YC. Decursinol and Decursin Protect Primary Cultured Rat Cortical Cells From Glutamate-induced Neurotoxicity. J Pharm Pharmacol. 2007;59(6):863-70. PubMed PMID: 17637179.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Decursinol and decursin protect primary cultured rat cortical cells from glutamate-induced neurotoxicity. AU - Kang,So Young, AU - Kim,Young Choong, PY - 2007/7/20/pubmed PY - 2007/10/5/medline PY - 2007/7/20/entrez SP - 863 EP - 70 JF - The Journal of pharmacy and pharmacology JO - J Pharm Pharmacol VL - 59 IS - 6 N2 - We previously reported six neuroprotective decursinol derivatives, coumarins from Angelica gigas (Umbelliferae) roots. To elucidate the action patterns of decursinol derivatives, we investigated the neuroprotective effects of decursinol and decursin, which showed highly significant activity and were major constituents of A. gigas, using primary cultures of rat cortical cells in-vitro. At concentrations of 0.1-10.0 microM, both decursinol and decursin exerted a significant neuroprotective activity pretreatment and throughout treatment. In addition, decursin had a neuroprotective impact in the post-treatment paradigm implying that decursin might possess different action mechanisms from that of decursinol in the protection of neurons against glutamate injury. Both decursinol and decursin effectively reduced the glutamate-induced increased intracellular calcium ([Ca(2+)](i)) in cortical cells, suggesting that these two coumarins may exert neuroprotection by reducing calcium influx by overactivation of glutamate receptors. This suggestion was supported by the result that decursinol and decursin protected neurons against kainic acid (KA)-induced neurotoxicity better than against that induced by N-methyl-D-aspartate (NMDA). Moreover, both decursinol and decursin significantly prevented glutamate-induced decreases in glutathione, a cellular antioxidant, and glutathione peroxidase activity. In addition, both compounds efficiently reduced the overproduction of cellular peroxide in glutamate-injured cortical cells. These results suggested that both decursinol and decursin protected primary cultured rat cortical cells against glutamate-induced oxidative stress by both reducing calcium influx and acting on the cellular antioxidative defence system. Moreover, decursin is considered to probably have a different action mechanism from that of decursinol in protecting cortical cells against glutamate injury. SN - 0022-3573 UR - https://www.unboundmedicine.com/medline/citation/17637179/Decursinol_and_decursin_protect_primary_cultured_rat_cortical_cells_from_glutamate_induced_neurotoxicity_ L2 - https://doi.org/10.1211/jpp.59.6.0013 DB - PRIME DP - Unbound Medicine ER -