Curcumin Attenuates Glial Cell Activation But Cannot Suppress Hippocampal CA3 Neuronal Cell Death in i.c.v. Kanic Acid Injection Model.
- Author:
Jaeyoung CHO
1
;
Pil Jae KONG
;
Wanjoo CHUN
;
Yeo Ok MOON
;
Yee Tae PARK
;
So Young LIM
;
Sung Soo KIM
Author Information
1. Department of Pharmacology, College of Medicine, Kangwon National University, Chunchon 200-701, Korea. ksslsy@kangwon.ac.kr
- Publication Type:Original Article
- Keywords:
Curcumin;
Kanic acid;
Glial activation;
Astrocyte;
Microglia
- MeSH:
Ammonia;
Animals;
Astrocytes;
Cell Death*;
Curcumin*;
Gliosis;
Glutamic Acid;
Hippocampus;
Kainic Acid;
Microglia;
Neuroglia*;
Neurons*;
Reactive Oxygen Species;
Seizures
- From:The Korean Journal of Physiology and Pharmacology
2003;7(6):307-310
- CountryRepublic of Korea
- Language:English
-
Abstract:
Kainic acid (KA) is a structural analogue of glutamate that interacts with specific presynaptic and postsynaptic receptors to potentiate the release and excitatory actions of glutamate. Systemic or intracerebroventricular (i.c.v.) administration of KA to experimental animals elicits multifocal seizures with a predominantly limbic localization, and results in neuronal death of cornu ammonia 1 (CA1), reactive gliosis and biochemical changes in the hippocampus and other limbic structures. Several lines of evidence suggest that reactive oxygen species (ROS) play a pivotal role in the pathogenesis of excitotoxic death by KA. Curcumin has been known to possess anti-oxidative and anti-inflammatory activities. In this study, the effects of curcumin on KA induced hippocampal cell death, reactive gliosis and biochemical changes in reactive glia were investigated by immunohistochemical methods. Our data demonstrated that curcumin attenuated KA-induced astroglial and microglial activation although it did not protect KA-induced hippocampal cell death.
