作者: M. Moriyama , A.R. Jayakumar , X.Y. Tong , M.D. Norenberg
DOI: 10.1002/JNR.22400
关键词: Traumatic brain injury 、 Cell biology 、 Swelling 、 Internal medicine 、 Kinase 、 Cell signaling 、 Oxidative stress 、 Endocrinology 、 Pathogenesis 、 Edema 、 Biology 、 Cell
摘要: Cytotoxic brain edema, usually a consequence of astrocyte swelling, is an important complication stroke, traumatic injury, hepatic encephalopathy, and other neurological disorders. Although mechanisms underlying swelling are not fully understood, oxidative stress (OS) has generally been considered factor in its pathogenesis. To better understand the mechanism(s) by which OS causes cell we examined potential involvement mitogen-activated protein kinases (MAPKs) this process. Cultures exposed to theoxidant H2O2 (10, 25, 50 μM) for different time periods (1–24 hr) significantly increased triphasic manner. Swelling was initially observed at 10 min (peaking 30 min), followed shrinkage 1 hr. A subsequent increase volume occurred approximately 6 hr, rise lasted least 24 caused activation MAPKs (ERK1/2, JNK p38-MAPK), whereas inhibition diminished induced 25 μM H2O2. These findings suggest that mediation following stress. © 2010 Wiley-Liss, Inc.