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Sinapic acid attenuates kainic acid-induced hippocampal neuronal damage in mice.
Neuropharmacology. 2010 Jul-Aug; 59(1-2):20-30.N

Abstract

Excitotoxin induces neurodegeneration via glutamatergic activation or oxidative stress, which means that the blockade of glutamate receptors and the scavenging of free radicals are potential therapeutic targets in neurodegenerative diseases. Sinapic acid (SA) has a GABA(A) receptor agonistic property and free radical scavenging activity. We investigated the neuroprotective effects of SA on kainic acid (KA)-induced hippocampal brain damage in mice. SA (10 mg/kg) by oral administration has an anticonvulsant effect on KA-induced seizure-like behavior. Moreover, SA (10 mg/kg) significantly attenuated KA-induced neuronal cell death in the CA1 and CA3 hippocampal regions when administered as late as 6 h after KA. In addition, flumazenil, a GABA(A) antagonist, blocked the effect of SA administered immediately after KA but not the effect of SA administered 6 h after KA. This late protective effect of SA was accompanied by reduced levels of reactive gliosis, inducible nitric oxide synthase expression, and nitrotyrosine formation in the hippocampus. In the passive avoidance task, KA-induced memory impairments were ameliorated by SA. These results suggest that the potential therapeutic effect of SA is due to its attenuation of KA-induced neuronal damage in the brain via its anti-convulsive activity through GABA(A) receptor activation and radical scavenging activity.

Authors+Show Affiliations

Department of Life and Nanopharmaceutical Sciences, Biomedical Science Institute, School of Medicine, Kyung Hee University, Seoul, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

20363233

Citation

Kim, Dong Hyun, et al. "Sinapic Acid Attenuates Kainic Acid-induced Hippocampal Neuronal Damage in Mice." Neuropharmacology, vol. 59, no. 1-2, 2010, pp. 20-30.
Kim DH, Yoon BH, Jung WY, et al. Sinapic acid attenuates kainic acid-induced hippocampal neuronal damage in mice. Neuropharmacology. 2010;59(1-2):20-30.
Kim, D. H., Yoon, B. H., Jung, W. Y., Kim, J. M., Park, S. J., Park, D. H., Huh, Y., Park, C., Cheong, J. H., Lee, K. T., Shin, C. Y., & Ryu, J. H. (2010). Sinapic acid attenuates kainic acid-induced hippocampal neuronal damage in mice. Neuropharmacology, 59(1-2), 20-30. https://doi.org/10.1016/j.neuropharm.2010.03.012
Kim DH, et al. Sinapic Acid Attenuates Kainic Acid-induced Hippocampal Neuronal Damage in Mice. Neuropharmacology. 2010 Jul-Aug;59(1-2):20-30. PubMed PMID: 20363233.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sinapic acid attenuates kainic acid-induced hippocampal neuronal damage in mice. AU - Kim,Dong Hyun, AU - Yoon,Byung Hoon, AU - Jung,Won Yong, AU - Kim,Jong Min, AU - Park,Se Jin, AU - Park,Dong Hyun, AU - Huh,Youngbuhm, AU - Park,Chan, AU - Cheong,Jae Hoon, AU - Lee,Kyung-Tae, AU - Shin,Chan Young, AU - Ryu,Jong Hoon, Y1 - 2010/04/02/ PY - 2008/12/29/received PY - 2010/01/27/revised PY - 2010/03/19/accepted PY - 2010/4/6/entrez PY - 2010/4/7/pubmed PY - 2010/10/21/medline SP - 20 EP - 30 JF - Neuropharmacology JO - Neuropharmacology VL - 59 IS - 1-2 N2 - Excitotoxin induces neurodegeneration via glutamatergic activation or oxidative stress, which means that the blockade of glutamate receptors and the scavenging of free radicals are potential therapeutic targets in neurodegenerative diseases. Sinapic acid (SA) has a GABA(A) receptor agonistic property and free radical scavenging activity. We investigated the neuroprotective effects of SA on kainic acid (KA)-induced hippocampal brain damage in mice. SA (10 mg/kg) by oral administration has an anticonvulsant effect on KA-induced seizure-like behavior. Moreover, SA (10 mg/kg) significantly attenuated KA-induced neuronal cell death in the CA1 and CA3 hippocampal regions when administered as late as 6 h after KA. In addition, flumazenil, a GABA(A) antagonist, blocked the effect of SA administered immediately after KA but not the effect of SA administered 6 h after KA. This late protective effect of SA was accompanied by reduced levels of reactive gliosis, inducible nitric oxide synthase expression, and nitrotyrosine formation in the hippocampus. In the passive avoidance task, KA-induced memory impairments were ameliorated by SA. These results suggest that the potential therapeutic effect of SA is due to its attenuation of KA-induced neuronal damage in the brain via its anti-convulsive activity through GABA(A) receptor activation and radical scavenging activity. SN - 1873-7064 UR - https://www.unboundmedicine.com/medline/citation/20363233/Sinapic_acid_attenuates_kainic_acid_induced_hippocampal_neuronal_damage_in_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(10)00088-2 DB - PRIME DP - Unbound Medicine ER -