請用此 Handle URI 來引用此文件: http://hdl.handle.net/11455/68153
標題: Indomethacin causes renal epithelial cell injury involving Mcl-1 down-regulation
作者: Ou, Y.C.
Yang, C.R.
Cheng, C.L.
Jian-Ri, U.
Raung, S.L.
Hung, Y.Y.
Chen, C.J.
關鍵字: Apoptosis
Indomethacin
Mcl-1
Mitochondria
nonsteroidal antiinflammatory drugs
celecoxib-induced apoptosis
neutrophil apoptosis
signaling pathway
cancer cells
inhibition
akt
mechanism
carcinoma
survival
期刊/報告no:: Biochemical and Biophysical Research Communications, Volume 380, Issue 3, Page(s) 531-536.
摘要: Nonsteroidal anti-inflammatory drugs (NSAIDs) exert anti-tumor action in a variety of cancer cells. However, several treatment side effects such is gastrointestinal injury, cardiovascular toxicity, and acute renal failure limit their clinical use. We found that indomethacin caused renal epithelial cell injury independently of cyclooxygenase inhibition. Indomethacin treatment was associated with the disruption Of mitochondrial transmembrane potential, release of cytochrome c, down-regulation of Bcl-2 and Mcl-1, up-regulation of Bax, and elevation of caspases activity, Enhanced Mcl-1 but not Bcl-2 expression alleviated indomethacin-increased caspase-3 activity. Down-regulation of Akt-related and signal transducer and activator of transcription (STAT-3)-related Pathways was found in indomethacin-treated cells. Pharmacological and genetic studies revealed a potential mechanistic link between Akt/Mcl-1 and STAT-3/Mcl-1 signaling pathways and indomethacin-induced cytotoxicity. Mcl-1 is a determinant molecule for the induction of epithelial cell injury caused by indomethacin. Therefore, the maintenance of Mcl-1 levels is important for prevention of renal epithelial cell injury and apoptosis. (C) 2009 Elsevier Inc. All rights reserved.
URI: http://hdl.handle.net/11455/68153
ISSN: 0006-291X
文章連結: http://dx.doi.org/10.1016/j.bbrc.2009.01.094
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