Background.Cyclophosphamide (CP) is a nitrogen mustard alkylating drug used for the treatment of chronic and acute malignant lymphomas, myeloma, leukemia, neuroblastoma, adenocarcinoma, retinoblastoma, breast carcinoma, and immunosuppressive therapy. Despite its vast therapeutic uses, it is known to cause severe cardiac toxicity. Kolaviron (KV), a Garcinia kola seed extract containing a mixture of flavonoids, is reputed for its antioxidant and membrane stabilizing properties.Objective.This study investigated the protective effect of KV on CP-induced cardiotoxicity in rats.Methods.Thirty rats were used, and they were divided into 6 groups of 5 rats each. Group I received 2 mL/kg propylene glycol orally for 14 days; group II received CP (50 mg/kg/d, intraperitoneally [i.p.]) for 3 days; groups III and IV received 200 and 400 mg/kg/d KV, respectively, orally for 14 days and groups V and VI were pretreated with 200 and 400 mg/kg/d KV, respectively, orally for 14 days followed by CP (50 mg/kg/d, i.p.) for 3 days.Results.CP treatment resulted in a significantly lower food consumption and body weight in rats. The lactate dehydrogenase and creatine kinase enzymes in cardiac tissues of rats treated with CP were significantly higher. In cardiac tissues, 3-day doses of CP resulted in significantly higher heart weight, cardiac troponin I, myeloperoxidase, malondialdehyde, hydrogen peroxide and lower superoxide dismutase, catalase, glutathione peroxidase activities, and reduced glutathione levels. Histological examination of cardiac tissues showed sign of necrosis of myocardium after CP treatment. However, administration of KV at 200 and 400 mg/kg for 14 days prior to CP treatment, increase food consumption, body weight, and attenuates the biochemical and histological changes induced by CP.Conclusions.These results revealed that KV attenuates CP-induced cardiotoxicity by inhibiting oxidative stress and preserving the activity of antioxidant enzymes.

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Diclofenac (DF) is widely used in the treatment of pain and fever. Despite it therapeutic benefits, it triggered hepatorenal injury. Thus, the present study investigated the protective roles of kolaviron (KV) against DF-induced hepatic and renal toxicity in rats. The rats were allotted into groups: control group received propylene glycol and treatment groups received DF, which induced hepatorenal toxicity in rats and different doses of KV that prevented systemic toxicity of DF in rats. Twenty-four hours after the last treatment, all the rats were killed. Pro-inflammatory levels, markers of liver and kidney functions, oxidative stress, hematological indices, and histopathological alterations were evaluated. Diclofenac caused significant increase in the plasma levels of creatinine and urea and activities of liver enzymes, including bilirubin level, pro-inflammatory markers, and plasma prostaglandin E2 (PGE2). It also caused significant alteration in renal and hepatic PGE2, antioxidants, lipid peroxidation (malondialdehyde), and hematological indices. These toxic effects were confirmed by histological studies and levels of inflammatory infiltration (myeloperoxidase). However, KV significantly prevented or reduced the adverse effects of DF in the plasma, liver, and kidney of the rats pretreated with KV before DF administration. This study showed the efficacy of KV as hepatic and renal protector in DF-induced hepatorenal toxicity through reduction of oxidative stress and suppression of inflammation.

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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 PGE release; 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 PGE release back to the basal levels.

The beneficial effects of Ocimum gratissimum, have been attributed mainly to its antioxidant and antiinflammatory properties. This study investigated the protective effects of aqueous extract of Ocimum gratissimum leaves (AEOGL) on acetic acid induced colitis in male rats. Twenty male Wistar rats, 100-180 g were divided into four groups as follows: Group 1 (control) (n = 5) received 2 ml/kg of distilled water for 21 consecutive days. Group 2 (n = 5) received 2 ml of 6% acetic acid solution once intra rectally for induction of colitis. Group 3 and 4 (n = 5 each) were treated as group 2 and thereafter received AEOGL orally at 200 and 400 mg/kg/day respectively for 20 consecutive days. All the animals from each group were sacrificed 24 h after the induction of colitis and administration of AEOGL. The diarrhea score, ulcer score, hematological parameters, nitric oxide (NO), myeloperoxidase (MPO), superoxide dismutase (SOD), reduced glutathione (GSH) markers and histopathological alteration were evaluated. Acetic acid-induced colitis significantly caused alteration in diarrhea score, ulcer score, hematological parameters, MPO and SOD activities, NO and GSH levels (p < 0.05). It induced significant inflammation of the colonic tissue. AEOGL administration significantly decreased diarrhea score and ulcer score to normal (p < 0.05). It prevented alteration effect of acetic acid on hematological parameters and significant decreases the activities of MPO, SOD, NO and increase GSH levels (p < 0.05) in colitis rats. In conclusion, Ocimum gratissimum leaves possesses ameliorative effects against acetic acid-induced colitis as a consequence of its antiinflammatory and anti-oxidative properties.

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