Tags

Type your tag names separated by a space and hit enter

Sesamin ameliorates oxidative stress and mortality in kainic acid-induced status epilepticus by inhibition of MAPK and COX-2 activation.
J Neuroinflammation. 2011 May 24; 8:57.JN

Abstract

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.

Authors+Show Affiliations

Division of Neurology, Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan. pfhsieh@vghtc.gov.twNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21609430

Citation

Hsieh, Peiyuan F., et al. "Sesamin Ameliorates Oxidative Stress and Mortality in Kainic Acid-induced Status Epilepticus By Inhibition of MAPK and COX-2 Activation." Journal of Neuroinflammation, vol. 8, 2011, p. 57.
Hsieh PF, Hou CW, Yao PW, et al. Sesamin ameliorates oxidative stress and mortality in kainic acid-induced status epilepticus by inhibition of MAPK and COX-2 activation. J Neuroinflammation. 2011;8:57.
Hsieh, P. F., Hou, C. W., Yao, P. W., Wu, S. P., Peng, Y. F., Shen, M. L., Lin, C. H., Chao, Y. Y., Chang, M. H., & Jeng, K. C. (2011). Sesamin ameliorates oxidative stress and mortality in kainic acid-induced status epilepticus by inhibition of MAPK and COX-2 activation. Journal of Neuroinflammation, 8, 57. https://doi.org/10.1186/1742-2094-8-57
Hsieh PF, et al. Sesamin Ameliorates Oxidative Stress and Mortality in Kainic Acid-induced Status Epilepticus By Inhibition of MAPK and COX-2 Activation. J Neuroinflammation. 2011 May 24;8:57. PubMed PMID: 21609430.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sesamin ameliorates oxidative stress and mortality in kainic acid-induced status epilepticus by inhibition of MAPK and COX-2 activation. AU - Hsieh,Peiyuan F, AU - Hou,Chien-Wei, AU - Yao,Pei-Wun, AU - Wu,Szu-Pei, AU - Peng,Yu-Fen, AU - Shen,Mei-Lin, AU - Lin,Ching-Huei, AU - Chao,Ya-Yun, AU - Chang,Ming-Hong, AU - Jeng,Kee-Ching, Y1 - 2011/05/24/ PY - 2010/12/14/received PY - 2011/05/24/accepted PY - 2011/5/26/entrez PY - 2011/5/26/pubmed PY - 2011/10/4/medline SP - 57 EP - 57 JF - Journal of neuroinflammation JO - J Neuroinflammation VL - 8 N2 - 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. SN - 1742-2094 UR - https://www.unboundmedicine.com/medline/citation/21609430/Sesamin_ameliorates_oxidative_stress_and_mortality_in_kainic_acid_induced_status_epilepticus_by_inhibition_of_MAPK_and_COX_2_activation_ L2 - https://jneuroinflammation.biomedcentral.com/articles/10.1186/1742-2094-8-57 DB - PRIME DP - Unbound Medicine ER -