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Oxidative toxicity in BV-2 microglia cells: sesamolin neuroprotection of H2O2 injury involving activation of p38 mitogen-activated protein kinase.
Ann N Y Acad Sci. 2005 May; 1042:279-85.AN

Abstract

Reactive oxygen species (ROS) has been proposed to play a pathogenic role in neuronal injury. Sesame antioxidants that inhibit lipid peroxidation and regulate cytokine production may suppress ROS generation. In this study, we focused on the effect of sesamolin on H2O2-induced neurotoxicity and ROS production in the murine microglial cell line BV-2. Results indicate that the H2O2 elicited BV-2 cell death in a concentration- and time-dependent manner. ROS generation in BV-2 cells was time-dependently increased by the H2O2 treatment. Sesamolin reduced ROS generation in BV-2 cells. p38 mitogen-activated protein kinase (MAPK) and caspase-3 were also activated in BV-2 cells under H2O2 stress. Sesamolin was able to inhibit H2O2-induced p38 MAPK and caspase-3 activation and cell death. In addition, sesamolin preserved superoxide dismutase and catalase activities in BV-2 cells under H2O2 stress. In conclusion, sesamolin protects microglia against H2O2-induced cell injury and this protective effect was accompanied by its inhibition of p38 MAPK and caspase-3 activation and ROS production.

Authors+Show Affiliations

Jen-Teh Junior College of Medical and Nursing Management, Miaoli, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15965073

Citation

Hou, Rolis Chien-Wei, et al. "Oxidative Toxicity in BV-2 Microglia Cells: Sesamolin Neuroprotection of H2O2 Injury Involving Activation of P38 Mitogen-activated Protein Kinase." Annals of the New York Academy of Sciences, vol. 1042, 2005, pp. 279-85.
Hou RC, Wu CC, Huang JR, et al. Oxidative toxicity in BV-2 microglia cells: sesamolin neuroprotection of H2O2 injury involving activation of p38 mitogen-activated protein kinase. Ann N Y Acad Sci. 2005;1042:279-85.
Hou, R. C., Wu, C. C., Huang, J. R., Chen, Y. S., & Jeng, K. C. (2005). Oxidative toxicity in BV-2 microglia cells: sesamolin neuroprotection of H2O2 injury involving activation of p38 mitogen-activated protein kinase. Annals of the New York Academy of Sciences, 1042, 279-85.
Hou RC, et al. Oxidative Toxicity in BV-2 Microglia Cells: Sesamolin Neuroprotection of H2O2 Injury Involving Activation of P38 Mitogen-activated Protein Kinase. Ann N Y Acad Sci. 2005;1042:279-85. PubMed PMID: 15965073.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidative toxicity in BV-2 microglia cells: sesamolin neuroprotection of H2O2 injury involving activation of p38 mitogen-activated protein kinase. AU - Hou,Rolis Chien-Wei, AU - Wu,Chia-Chuan, AU - Huang,Jing-Rong, AU - Chen,Yuh-Shuen, AU - Jeng,Kee-Ching G, PY - 2005/6/21/pubmed PY - 2006/9/12/medline PY - 2005/6/21/entrez SP - 279 EP - 85 JF - Annals of the New York Academy of Sciences JO - Ann N Y Acad Sci VL - 1042 N2 - Reactive oxygen species (ROS) has been proposed to play a pathogenic role in neuronal injury. Sesame antioxidants that inhibit lipid peroxidation and regulate cytokine production may suppress ROS generation. In this study, we focused on the effect of sesamolin on H2O2-induced neurotoxicity and ROS production in the murine microglial cell line BV-2. Results indicate that the H2O2 elicited BV-2 cell death in a concentration- and time-dependent manner. ROS generation in BV-2 cells was time-dependently increased by the H2O2 treatment. Sesamolin reduced ROS generation in BV-2 cells. p38 mitogen-activated protein kinase (MAPK) and caspase-3 were also activated in BV-2 cells under H2O2 stress. Sesamolin was able to inhibit H2O2-induced p38 MAPK and caspase-3 activation and cell death. In addition, sesamolin preserved superoxide dismutase and catalase activities in BV-2 cells under H2O2 stress. In conclusion, sesamolin protects microglia against H2O2-induced cell injury and this protective effect was accompanied by its inhibition of p38 MAPK and caspase-3 activation and ROS production. SN - 0077-8923 UR - https://www.unboundmedicine.com/medline/citation/15965073/Oxidative_toxicity_in_BV_2_microglia_cells:_sesamolin_neuroprotection_of_H2O2_injury_involving_activation_of_p38_mitogen_activated_protein_kinase_ L2 - https://doi.org/10.1196/annals.1338.050 DB - PRIME DP - Unbound Medicine ER -