Korean J Physiol Pharmacol 2010; 14(5): 257-263
Published online October 31, 2010 https://doi.org/10.4196/kjpp.2010.14.5.257
Copyright © Korean J Physiol Pharmacol.
Min-Soo Kwon2,*, Jin-Koo Lee1,*, Soo-Hyun Park1, Yun-Beom Sim1, Jun-Sub Jung1, Moo-Ho Won3, Seon-Mi Kim1, and Hong-Won Suh1
1Department of Pharmacology, Institute of Natural Medicine, College of Medicine, Hallym University, Chuncheon 200-702, 2Department of Aerospace Medical Research, Aerospace Medical Center, ROKAF (Republic of Korea Air Force), Cheongwon 363-842, 3Department of Anatomy and Neurobiology, and Institute of Neurodegeneration and Neuroregeneration, College of Medicine, Hallym University, Chuncheon 200-702, Korea
Visnagin (4-methoxy-7-methyl-5H-furo[3,2-g][1]-benzopyran-5-one), which is an active principle extracted from the fruits of Ammi visnaga, has been used as a treatment for low blood-pressure and blocked blood vessel contraction by inhibition of calcium influx into blood cells. However, the neuroprotective effect of visnagin was not clearly known until now. Thus, we investigated whether visnagin has a neuroprotective effect against kainic acid (KA)-induced neuronal cell death. In the cresyl violet staining, pre-treatment or post-treatment visnagin (100 mg/kg, p.o. or i.p.) showed a neuroprotective effect on KA (0.1Ռg) toxicity. KA-induced gliosis and proinflammatory marker (IL-1Ղ, TNF-Ձ, IL-6, and COX-2) inductions were also suppressed by visnagin administration. These results suggest that visnagin has a neuroprotective effect in terms of suppressing KA-induced pathogenesis in the brain, and that these neuroprotective effects are associated with its anti-inflammatory effects.
Keywords: Neuroprotection, Kainic acid, Hippocampus, Visnagin, Cytokines
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