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Fattori, V., Sergio Borghi, M., Carla Guazelli, F.S., Andressa Giroldo, C., Crespigio, J., Allan Bussmann, J.C., Coelho-Silva, L., Natasha Ludwig, G., Tania Mazzuco, G., Casagrande, R. and Waldiceu Verri Jr., A. (2017) Vinpocetine Reduces Diclofenac-Induced Acute Kidney Injury through Inhibition of Oxidative Stress, Apoptosis, Cytokine Production, and NF-κB Activation in Mice. Pharmacological Research, 120, 10-22.
https://doi.org/10.1016/j.phrs.2016.12.039
has been cited by the following article:
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TITLE:
Diclofenac-Induced Kidney Damage in Wistar Rats: Involvement of Antioxidant Mechanism
AUTHORS:
Tijani S. Abiola, Oyindamola C. Adebayo, O. O. Babalola
KEYWORDS:
Orogastrically, Oxidative Stress, Toxicity, Diclofenac, Kidney Damage
JOURNAL NAME:
Journal of Biosciences and Medicines,
Vol.7 No.12,
December
2,
2019
ABSTRACT: Kidney damage has been associated with administration diclofenac, a phenylacetic acid derivative belonging to the nonsteroidal anti-inflammatory drugs (NSAIDs), which is commonly used for the treatment of various diseases such as rheumatoid arthritis, ankylosing spondylitis, acute muscle pain conditions and osteoarthritis. This study investigated the exact mechanism of diclofenac in renal toxicity by determining the involvement of oxidative stress in rats. Adult male Wistar rats were divided into two groups of eight rats in each group and orogastrically treated for three days. Group 1 served as the normal control and received normal saline (0.9% w/v) and group 2 received 40 mg/kg body weight of diclofenac for three days. Administration of diclofenac caused degeneration of the kidney of rats as evidenced by significant elevation in the serum levels of creatinine, urea, albumin, uric acid, protein and electrolytes and the activities of renal-5’-nucleotidase and glucose-6-phosphate-dehydrogenase (G6PDH) compared with control. Furthermore, administration of diclofenac decreased the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glutathione-S-transferase (GST) and the level of glutathione with concomitant increase in hydrogen peroxide (H2O2) and malondialdehyde (MDA) levels in the kidney of the diclofenac treated groups compared with control. These findings reveal that administration of diclofenac may impair kidney functions through induction of oxidative stress.