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https://doi.org/10.1016/j.bbrc.2008.02.116
Title: | Nephrotoxic cell death by diclofenac and meloxicam | Authors: | Ng, L.E. Halliwell, B. Wong, K.P. |
Keywords: | Apoptosis Caspase Cytochrome c Diclofenac LLC-PK1 MDCKII Meloxicam |
Issue Date: | 2008 | Citation: | Ng, L.E., Halliwell, B., Wong, K.P. (2008). Nephrotoxic cell death by diclofenac and meloxicam. Biochemical and Biophysical Research Communications 369 (3) : 873-877. ScholarBank@NUS Repository. https://doi.org/10.1016/j.bbrc.2008.02.116 | Abstract: | The nephrotoxicity of diclofenac, a non-steroidal anti-inflammatory drug that inhibits both isoforms of cyclooxygenase (COX) has been reported to be fatal to vultures but this was not so with meloxicam which is COX-2 selective. Our study showed that diclofenac was more toxic than meloxicam to both the proximal tubular LLC-PK1 cells and the distal tubular Madin-Darby canine kidney type II (MDCKII) cells, and that LLC-PK1 cells were more susceptible. Exposure of MDCKII cells to meloxicam caused activation of caspase-9/-3 and release of cytochrome c. These observations together with a positive annexin V-FITC staining implicate an intrinsic mitochondrial cell death pathway by apoptosis. Diclofenac-treated MDCKII cells on the other hand showed extensive propidium iodide staining, suggestive of cell death by necrosis. The mode of cell death in LLC-PK1 cells was however less well-defined with positive annexin V-FITC staining but minimal increase in caspase-3 activity alluding to a caspase-independent pathway. © 2008 Elsevier Inc. All rights reserved. | Source Title: | Biochemical and Biophysical Research Communications | URI: | http://scholarbank.nus.edu.sg/handle/10635/28621 | ISSN: | 0006291X 10902104 |
DOI: | 10.1016/j.bbrc.2008.02.116 |
Appears in Collections: | Staff Publications |
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