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DC Field | Value | Language |
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dc.contributor.author | Nusuetrong P. | |
dc.contributor.author | Pengsuparp T. | |
dc.contributor.author | Meksuriyen D. | |
dc.contributor.author | Tanitsu M. | |
dc.contributor.author | Kikuchi H. | |
dc.contributor.author | Mizugaki M. | |
dc.contributor.author | Shimazu K.-I. | |
dc.contributor.author | Oshima Y. | |
dc.contributor.author | Nakahata N. | |
dc.contributor.author | Yoshida M. | |
dc.date.accessioned | 2021-04-05T04:31:59Z | - |
dc.date.available | 2021-04-05T04:31:59Z | - |
dc.date.issued | 2008 | |
dc.identifier.issn | 9186158 | |
dc.identifier.other | 2-s2.0-45749109056 | |
dc.identifier.uri | https://ir.swu.ac.th/jspui/handle/123456789/14856 | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-45749109056&doi=10.1248%2fbpb.31.1115&partnerID=40&md5=e1e4a9d282e4055287d49b2a3ecb96ee | |
dc.description.abstract | Satratoxin H, a mycotoxin, is thought to induce apoptosis of PC12 cells through the activation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) in a glutathione (GSH)-sensitive manner. The present study was undertaken to further elucidate the mechanism by which satratoxin H induces cell death in PC12 cells. Satratoxin H caused apoptosis of PC12 cells within 24-h, as determined by DNA fragmentation and flow cytometric analysis. Satratoxin H increased reactive oxygen species (ROS) production and lipid peroxidation, as determined by malondialdehyde formation. These effects were attenuated by incubation of cells with GSH, suggesting that satratoxin H-induced increase in apoptosis of serum-deprived PC12 cells may be partially mediated through the generation of ROS. © 2008 Pharmaceutical Society of Japan. | |
dc.subject | glutathione | |
dc.subject | lipid peroxide | |
dc.subject | malonaldehyde | |
dc.subject | mycotoxin | |
dc.subject | reactive oxygen metabolite | |
dc.subject | satratoxin h | |
dc.subject | animal cell | |
dc.subject | apoptosis | |
dc.subject | article | |
dc.subject | cell viability | |
dc.subject | controlled study | |
dc.subject | DNA fragmentation | |
dc.subject | drug effect | |
dc.subject | drug mechanism | |
dc.subject | flow cytometry | |
dc.subject | lipid peroxidation | |
dc.subject | nonhuman | |
dc.subject | pheochromocytoma | |
dc.subject | rat | |
dc.subject | Animals | |
dc.subject | Antioxidants | |
dc.subject | Cell Survival | |
dc.subject | DNA Fragmentation | |
dc.subject | Electrophoresis, Agar Gel | |
dc.subject | Flow Cytometry | |
dc.subject | G1 Phase | |
dc.subject | Glutathione | |
dc.subject | Indicators and Reagents | |
dc.subject | JNK Mitogen-Activated Protein Kinases | |
dc.subject | Lipid Peroxidation | |
dc.subject | p38 Mitogen-Activated Protein Kinases | |
dc.subject | PC12 Cells | |
dc.subject | Rats | |
dc.subject | Reactive Oxygen Species | |
dc.subject | Thiobarbituric Acid Reactive Substances | |
dc.subject | Trichothecenes | |
dc.title | Satratoxin H generates reactive oxygen species and lipid peroxides in PC12 cells | |
dc.type | Article | |
dc.rights.holder | Scopus | |
dc.identifier.bibliograpycitation | Biological and Pharmaceutical Bulletin. Vol 31, No.6 (2008), p.1115-1120 | |
dc.identifier.doi | 10.1248/bpb.31.1115 | |
Appears in Collections: | Scopus 1983-2021 |
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