The neuroprotective effects of the seeds of Cassia obtusifolia on transient cerebral global ischemia in mice

author Dong Hyun Kim, Sunho Kim, Won Yong Jung, Se Jin Park, Dong Hyun Park, Jong Min Kim, Jae Hoon Cheong, Jong Hoon Ryu
his workplace 1Department of Life and Nanopharmaceutical Sciences, Kyung Hee University, #1 Hoeki-dong, Dongdaemoon-Ku, Seoul 130-701, Republic of Korea2Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University, #1 Hoeki-dong, Dongdeamoon-ku, Seoul 130-701, Republic of Korea3Kyung Hee East-West Pharmaceutical Research Institute, College of Pharmacy, Kyung Hee University, #1 Hoeki-dong, Dongdaemoon-Ku, Seoul 130-701, Republic of Korea4Department of Pharmacy, Sahmyook University, Nowon-goo, Seoul 139-742, Republic of Korea
periodicalFood and Chemical Toxicology, 2009, Vol.47 (7), pp.1473-1479
sourceElsevier Journal
DOI10.1016/j.fct.2009.03.028
key word Global ischemia; Glia; iNOS; COX-2; BDNF; pCREB;
abstractAbstract(#br)The aim of this study was to determine the mechanism underlying the neuroprotective effects of the ethanolic extract of the seeds of Cassia obtusifolia (COE) (10 or 50mg/kg/day, p.o) on transient cerebral global ischemia induced by bilateral common carotid artery occlusion (2VO) in mice. Immunohistochemical and western blot studies showed that levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the hippocampal CA1 region at 1day post-2VO were attenuated by COE (50mg/kg/day, p.o), which was administered immediately after 2VO. Furthermore, OX-42 – and glial fibrillary acidic protein (GFAP)-positive cell numbers at 4days post-2VO were markedly attenuated by COE (50 sp="0.25"/>mg/kg/day, p.o) treatment for 4days in CA1. Viable neurons detected by Nissl at 7days post-2VO were increased by administering COE (50mg/kg/day, p.o) for 7days. In addition, COE increased the expressions of phosphorylated cAMP response element binding protein (CREB) and brain-derived neurotrophic factor (BDNF) in CA1 in na?ve-control within 1 and 6h, respectively, and these expressions were also profoundly increased in 2VO-treated mice by COE at immediately post-2VO. These results suggest that the neuroprotective effects of COE are due to its anti-inflammatory effects and to its upregulation of BDNF expression and CREB phosphorylation.
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