Abstract Title:

Kolaviron attenuates diclofenac-induced nephrotoxicity in male Wistar rats.

Abstract Source:

Appl Physiol Nutr Metab. 2018 Sep ;43(9):956-968. Epub 2018 May 30. PMID: 29847737

Abstract Author(s):

Quadri K Alabi, Rufus O Akomolafe, Modinat A Adefisayo, Olaoluwa S Olukiran, Aliyat O Nafiu, Micheal K Fasanya, Ayowole A Oladele

Article Affiliation:

Quadri K Alabi


The beneficial effects of kolaviron, a natural biflavonoid from the seeds of Garcinia kola, have been attributed to its antioxidant and anti-inflammatory activities. This study was designed to investigate the renoprotective effect of kolaviron in rat model of diclofenac (DFC)-induced acute renal failure. Thirty-five male Wistar rats were divided into 7 groups of 5 rats each as follows: a control group that received propylene glycol orally and treatment groups that received DFC, DFC recovery, DFC followed by kolaviron at 3 different doses, and kolaviron only. DFC-treated rats showed sluggishness, illness, and anorexia. Their urine contained appreciable protein, glucose, and ketone bodies. Histopathological examination of their kidneys revealed profound acute tubular necrosis. DFC treatment significantly increased levels of plasma creatinine, urea, sodium, chloride, potassium ions, and increased renal tissue activities of superoxide dismutase, catalase, levels of malondialdehyde, and hydrogen peroxide. Fractional excretion of sodium and potassium and renal tissue levels of reduced glutathione and prostaglandin E(PGE) decreased significantly in DFC-treated groups. However, kolaviron administration significantly reduced the toxic effect of DFC on PGErelease; plasma levels of creatinine, urea, glucose, and electrolytes; and significantly attenuated renal tubular and oxidative damages. Furthermore, the effects of DFC administration on food consumption, water intake, urine output and urine protein, glucose, ketone bodies, and electrolytes were significantly attenuated in animals treated with kolaviron. The results suggested that kolaviron ameliorated DFC-induced kidney injury in Wistar rats by decreasing renal oxidative damage and restoration of renal PGErelease back to the basal levels.

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