Protective effect of a sesamin derivative, 3-bis 3-methoxybenzyl butane-1, 4-diol on ischemic and hypoxic neuronal injuryReportar como inadecuado

Protective effect of a sesamin derivative, 3-bis 3-methoxybenzyl butane-1, 4-diol on ischemic and hypoxic neuronal injury - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

Journal of Biomedical Science

, 21:15

First Online: 18 February 2014Received: 22 November 2013Accepted: 17 February 2014DOI: 10.1186-1423-0127-21-15

Cite this article as: Hou, CW., Chen, YL., Chuang, SH. et al. J Biomed Sci 2014 21: 15. doi:10.1186-1423-0127-21-15


BackgroundStroke is one of the leading causes of neuronal death. Sesamin is known for neuroprotection by its antioxidant and anti-inflammatory properties but it lacks blood–brain barrier BBB activity. A panel of sesamin derivatives was screened and 3-bis 3-methoxybenzyl butane-1,4-diol BBD was selected for high BBB activity and tested for its neuroprotective effect.

MethodsThe focal cerebral ischemia of Sprague–Dawley rats and hypoxia models of murine BV-2 microglia or PC12 cells under oxygen-glucose deprivation were used for in vivo and in vitro test, respectively. Lipid peroxidation and superoxide dismutase SOD activity from the ischemic brain were tested and reactive oxygen species ROS, cytokine production, prostaglandin PGE2 and related signaling pathways from hypoxic cells were examined by ELISA or Western blot assay, respectively.

ResultsBBD showed a protective effect when given 90 min after the focal cerebral ischemia. It also reduced lipid peroxidation and preserved SOD activity from the ischemic brain. The mechanism of BBD was further confirmed by attenuating ROS, cytokine production, and PGE2 release from hypoxic BV-2 or PC12 cells. BBD significantly reduced hypoxia-induced c-Jun N-terminal kinases JNK and modulated AKT-1 and caspase-3 survival and apoptotic pathways in BV-2 cells, and inhibited hypoxia-induced JNK and cyclooxygenase-2 activation in PC12 cells.

ConclusionsThe neuroprotective effect of BBD on ischemia-hypoxia models was involved with antioxidant and anti-inflammatory effects. The result would help the development of new CNS drug for protection of ischemia-hypoxia injury.

KeywordsCerebral ischemia Hypoxia Neuroprotection Sesamin derivative Membrane permeability AbbreviationsMTT3-4,5-dimethyl-thiazol-2-yl-2,5-diphenyl tetrazolium bromide

BBD3-bis 3-methoxybenzyl butane-1,4-diol

JNKc-Jun N-terminal kinase


ERKExtracellular signal-regulated kinase

p38 MAPKp38 mitogen-activated protein kinase

PGE2Prostaglandin E2

hypoxiaOxygen-glucose deprivation

ROSReactive oxygen species

SODSuperoxide dismutase.

Electronic supplementary materialThe online version of this article doi:10.1186-1423-0127-21-15 contains supplementary material, which is available to authorized users.

Chien-Wei Hou, Yi-Ling Chen contributed equally to this work.

Download fulltext PDF

Autor: Chien-Wei Hou - Yi-Ling Chen - Shih-Hsien Chuang - Jen-Shu Wang - Kee-Ching Jeng


Documentos relacionados