Sesamin ameliorates oxidative stress and mortality in kainic acid-induced status epilepticus by inhibition of MAPK and COX-2 activation
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- 作者：Peiyuan F Hsieh (1) (2)
Chien-Wei Hou (3)
Pei-Wun Yao (3)
Szu-Pei Wu (3)
Yu-Fen Peng (3)
Mei-Lin Shen (1)
Ching-Huei Lin (1)
Ya-Yun Chao (1)
Ming-Hong Chang (1)
Kee-Ching Jeng (4) (5) - 关键词：Status epilepticus ; PC12 cells ; BV ; 2 cells ; sesamin ; kainic acid ; reactive oxygen species ; thiobarbituric acid reactive substances ; nitric acid ; superoxide dismutase ; mitogen ; activated protein kinases ; COX ; 2
- 刊名：Journal of Neuroinflammation
- 出版年：2011
- 出版时间：December 2011
- 年：2011
- 卷：8
- 期：1
- 全文大小：544KB
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Chien-Wei Hou (3)
Pei-Wun Yao (3)
Szu-Pei Wu (3)
Yu-Fen Peng (3)
Mei-Lin Shen (1)
Ching-Huei Lin (1)
Ya-Yun Chao (1)
Ming-Hong Chang (1)
Kee-Ching Jeng (4) (5)
1. Division of Neurology, Taichung Veterans General Hospital, Taichung, Taiwan
2. Graduate Institute of Biomedicine and Biomedical Technology, National Chi Nan University, Nantou, Taiwan
3. Department of Biotechnology, Yuanpei University, Hsinchu, Taiwan
4. Department of Physical Education Office, Yuanpei University, Hsinchu, Taiwan
5. Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan - ISSN：1742-2094
文摘
Background Kainic acid (KA)-induced status epilepticus (SE) was involved with release of free radicals. Sesamin is a well-known antioxidant from sesame seeds and it scavenges free radicals in several brain injury models. However the neuroprotective mechanism of sesamin to KA-induced seizure has not been studied. Methods Rodents (male FVB mice and Sprague-Dawley rats) were fed with sesamin extract (90% of sesamin and 10% sesamolin), 15 mg/kg or 30 mg/kg, for 3 days before KA subcutaneous injection. The effect of sesamin on KA-induced cell injury was also investigated on several cellular pathways including neuronal plasticity (RhoA), neurodegeneration (Caspase-3), and inflammation (COX-2) in PC12 cells and microglial BV-2 cells. Results Treatment with sesamin extract (30 mg/kg) significantly increased plasma α-tocopherol level 50% and 55.8% from rats without and with KA treatment, respectively. It also decreased malondialdehyde (MDA) from 145% to 117% (p = 0.017) and preserved superoxide dismutase from 55% of the vehicle control mice to 81% of sesamin-treated mice, respectively to the normal levels (p = 0.013). The treatment significantly decreased the mortality from 22% to 0% in rats. Sesamin was effective to protect PC12 cells and BV-2 cells from KA-injury in a dose-dependent manner. It decreased the release of Ca2+, reactive oxygen species, and MDA from PC12 cells. Western blot analysis revealed that sesamin significantly reduced ERK1/2, p38 mitogen-activated protein kinases, Caspase-3, and COX-2 expression in both cells and RhoA expression in BV-2 cells. Furthermore, Sesamin was able to reduce PGE2 production from both cells under KA-stimulation. Conclusions Taken together, it suggests that sesamin could protect KA-induced brain injury through anti-inflammatory and partially antioxidative mechanisms.