Kolaviron Diminishes Diclofenac-Induced Liver and Kidney Toxicity inWistar Rats Via Suppressing Inflammatory Events Upregulating AntioxidantDefenses and Improving Hematological Indices

摘要

Diclofenac (DF) is widely used in the treatment of pain and fever. Despite ittherapeutic benefits, it triggered hepatorenal injury. Thus, the present studyinvestigated the protective roles of kolaviron (KV) against DF-induced hepaticand renal toxicity in rats. The rats were allotted into groups: control groupreceived propylene glycol and treatment groups received DF, which inducedhepatorenal toxicity in rats and different doses of KV that prevented systemictoxicity of DF in rats. Twenty-four hours after the last treatment, all the ratswere killed. Pro-inflammatory levels, markers of liver and kidney functions,oxidative stress, hematological indices, and histopathological alterations wereevaluated. Diclofenac caused significant increase in the plasma levels ofcreatinine and urea and activities of liver enzymes, including bilirubin level,pro-inflammatory markers, and plasma prostaglandin E (PGE ). It also caused significant alteration in renal andhepatic PGE , antioxidants, lipid peroxidation (malondialdehyde), andhematological indices. These toxic effects were confirmed by histologicalstudies and levels of inflammatory infiltration (myeloperoxidase). However, KVsignificantly prevented or reduced the adverse effects of DF in the plasma,liver, and kidney of the rats pretreated with KV before DF administration. Thisstudy showed the efficacy of KV as hepatic and renal protector in DF-inducedhepatorenal toxicity through reduction of oxidative stress and suppression ofinflammation.