(b).

NSAIDs coxibs	Sources of ROS generation	Cells/models/animals studied	Outcomes	References
Ibuprofen, ketoprofen, and indomethacin	Cytochrome P450 enzymes	Bacillus megaterium	All the NSAIDs caused a marked increase in the total cytochrome P450 level	[142]
Aspirin, diclofenac, diflunisal, flurbiprofen, ibuprofen, indomethacin, ketoprofen, mefenamic acid, naproxen, piroxicam, sulindac, and tolmetin	Cytochrome P450 enzymes	Rat hepatocytes	Cytotoxicity of diclofenac, ketoprofen, and piroxicam was increased by cytochrome P450 causing hepatotoxicity	[138]
Diclofenac and naproxen	Endothelial nitric oxide synthase	Spontaneous hypertensive rats	Increased expression of eNOS mRNA due to the generation of H2O2 which is responsible for upregulation of eNOS at the transcriptional and post-transcriptional levels	[114]
Rofecoxib and celecoxib	NADPH oxidases	Spontaneous hypertensive rats	NADPH expression increased in the heart and aorta by rofecoxib and celecoxib	[114]
		Human EA.hy 926 Endothelial cells	Nox2 Expression increased by rofecoxib	[114]
Rofecoxib and celecoxib	Endothelial nitric oxide synthase	Spontaneous hypertensive rats	In the aorta, the coxibs did not show any eNOS mRNA expression. In the heart only rofecoxib showed a significant increase in the expression of eNOS	[114]
Etodolac	ND	Human gastric epithelial cell line AGS	Increased apoptotic DNA fragmentation and expression of COX-2 mRNA	[79]
Nimesulide	NADPH oxidases	Rat adipocytes	Activation of NOX 4 isoform of NADPH oxidase results in the generation of H2O2	[115]

^*Although other reports are available suggesting the role of NSAIDs in ROS formation, the table lists only those NSAIDs for which results show that these NSAIDs are associated with CVD or NSAIDs mentioned in the text.