Cefepime and diclofenac sodium combined treatment-potentiated multiple organ injury: Role of oxidative damage and disrupted lipid metabolism.
Mohamed AboubakrAfaf AbdelkaderOla A HabottaNisreen AdelMahmoud A EmamEhab Y AbdelhieeObeid ShanabKhaled ShoghyHeba ElnouryMohamed M SolimanSamah F IbrahimAhmed AbdeenPublished in: Journal of biochemical and molecular toxicology (2021)
Concurrent exposure to antimicrobial and nonsteroidal anti-inflammatory drugs (NSAIDs) is usually inevitable in most infections and postsurgery. Consequently, the present study was designed to assess the intertwining impact of coadministration of cefepime (CP, a wide spectrum antibiotic) and diclofenac sodium (DF, an NSAID) on rat's liver, kidney, and testes. Rats received saline, CP (180 mg/kg/day, IM), DF (10 mg/kg/day, IM), or a combination of CP and DF. After 14 days, CP or DF induced tissue damage expressed by marked biochemical alterations in hepatic and renal function tests. Besides this, disrupted lipid metabolism and testosterone levels along with significant histological changes in hepatic, renal, and testicular tissues were noticed. A significant increase in malondialdehyde and decreases in superoxide dismutase and catalase activities alongside significant upregulated caspase 3 expression in tissues following CP or DF treatment suggested a bearable influence of oxidative stress, lipid peroxidation, and cell death. Accordingly, the simultaneous therapy of CP and DF evoked more obvious tissue damage than their individual treatment. Overall, data concluded that concurrent use of CP and DF in medical practice is a worrisome matter, so it should be done cautiously to avoid synergistic deleterious outcomes.
Keyphrases
- oxidative stress
- cell death
- healthcare
- gene expression
- diabetic rats
- replacement therapy
- primary care
- stem cells
- squamous cell carcinoma
- metabolic syndrome
- poor prognosis
- radiation therapy
- type diabetes
- mesenchymal stem cells
- electronic health record
- signaling pathway
- high glucose
- insulin resistance
- binding protein
- cancer therapy
- resting state
- smoking cessation
- drug induced
- endothelial cells
- big data
- cell cycle arrest
- heat stress