Please use this identifier to cite or link to this item: 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
Source: 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
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