Curcumin attenuates the kainic acid-induced hippocampal cell death in the mice

• Published in: Neuroscience letters 2007-04, Vol.416 (1), p.49-54
• Main Authors: Shin, Hyun Joo, Lee, Ji Yeong, Son, Eunyung, Lee, Dong Hun, Kim, Hyun Joon, Kang, Sang Soo, Cho, Gyeong Jae, Choi, Wan Sung, Roh, Gu Seob
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants - pharmacology; Astrocyte; Astrocytes - cytology; Astrocytes - drug effects; Astrocytes - metabolism; Biological and medical sciences; Caspase 3 - metabolism; Cell Death - drug effects; Curcumin; Curcumin - pharmacology; Enzyme Inhibitors - pharmacology; Excitatory Amino Acid Agonists - toxicity; Fundamental and applied biological sciences. Psychology; Glial Fibrillary Acidic Protein - metabolism; Heme Oxygenase-1 - metabolism; Hippocampus; Hippocampus - cytology; Immunohistochemistry; Kainic acid; Kainic Acid - toxicity; Male; Mice; Mice, Inbred ICR; Nitric Oxide Synthase Type II - metabolism; Nitric Oxide Synthase Type III; Oxidative Stress - drug effects; Vertebrates: nervous system and sense organs
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2007.01.060

Kainic acid (KA) induced oxidative stress is associated with hippocampal cell death. Recent studies suggest that curcumin, a potent antioxidant, may provide protection for KA-induced oxidative stress. We investigated the effects of curcumin treatment on hippocampal reactive astrocytes in mice with KA-induced seizures. Eighteen hours after curcumin treatment, mice were treated with KA (30 mg/kg, i.p.), and then sacrificed after a further 48 h. Using cresyl violet staining and TUNEL analysis, histological evaluation revealed cell death in the KA-treated hippocampus. However, marked cell death was not observed in mice treated with curcumin. In addition, curcumin treatment reduced the KA-induced immunoreactivity of caspase-3. Similarly, immunoreactivity analyses indicated that KA causes upregulation of hippocampal GFAP, eNOS, and HO-1 levels, all of which were reduced in animals those received the curcumin treatment. Our findings indicate that curcumin is a potent inhibitor of reactive astrocyte expression and thus, prevents hippocampal cell death. These results also support its potential for use in the treatment of neurodegenerative diseases.