3 research outputs found

    Ocimum gratissimum Ameliorates Gentamicin-Induced Kidney Injury but Decreases Creatinine Clearance Following Sub-Chronic Administration in Rats

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    The effects of aqueous extract of Ocimum gratissimum leaf (AOGL) on the renal function of rats with gentamicin-induced nephrotoxicity were investigated. This study involved the use of forty five (45) adult male Wistar rats (housed in separate metabolic cages) such that graded doses of OAGL were administered to the experimental groups (p.o.) for 28 days after exposure to gentamicin toxicity (100 mg/kg i.p.) for 1 week. At the end of the study, comparisons of some indices of renal function as well as antioxidant status (GSH and TBARS) were made between the control, toxic and AOGL-treated groups at P < 0.05. The result showed that gentamicin treatment caused significant increase (P < .05) in urine output, urea, creatinine, total protein, relative kidney weight, and TBARS, as well as significant decrease (P < .05) in urine creatinine and GSH levels. Post-treatment with graded doses of AOGL caused significant increase in food consumption, GSH, urine, and plasma creatinine, as well as significant decrease (P < .05) in relative kidney weight, TBARS, and urine total protein. There was an appreciable difference in the kidney histology of the AOGL-treated groups when compared with the toxic control. Hence, the extract has therapeutic potential in the management of gentamicin-induced kidney injury, although a risk profile of renal dysfunction is not unlikely from 28 days of administration as evident by the decrease in creatinine clearance

    Livolin Forte Ameliorates Cadmium-Induced Kidney Injury in Wistar Rats

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    The kidney, which is an integral part of the drug excretion system, was reported as one of the targets of cadmium toxicity. Early events of cadmium toxicity in the cell include a decrease in cell membrane fluidity, breakdown of its integrity, and impairment of its repair mechanisms. Phosphatidylcholine and vitamin E have a marked fluidizing effect on cellular membranes. We hypothesized that Livolin forte (LIV) could attenuate kidney damage induced by cadmium in rats. Twenty-five adult male Wistar rats were divided into five groups of five rats each: group I (control group) received 0.3 ml/kg/day of propylene glycol for six weeks; group II was given 5 mg/kg/day of cadmium (Cd) i.p for 5 consecutive days; group III rats were treated in a similar way as group II but were allowed a recovery period of 4 weeks; group IV was treated with LIV (5.2 mg/kg/day) for a period of 4 weeks after inducing renal injury with Cd similarly to group II; and group V was allowed a recovery period of 2 weeks after a 4-week LIV treatment (5.2 mg/kg/day) following Cd administration. A significant increase in plasma creatinine, urea, uric acid, and TBARS were observed in groups II and III compared to the control rats. Significant reductions in total protein, glucose, and GSH activity were also recorded. The urine concentrations of creatinine, urea, and uric acid in groups II and III were significantly lower than the control group. Th is finding was accompanied by a significant decrease in creatinine and urea clearance. Post-treatment with LIV caused significant decreases in plasma creatinine, urea, uric acid, and TBARS. Significant increases in total protein, glucose, and GSH activity of groups IV and V were observed compared to group II. A significant increase in urine concentrations of creatinine, urea, and uric acid and significant decreases in total protein, glucose, and GSH activity were observed in groups IV and V compared to group II. Photomicrographs of the rat kidneys in groups IV and V showed an improvement in the histology of their renal tissue when compared to group II, with features similar to the control rats. Additionally, group III showed an improvement in the histoarchitecture of the kidney compared with group II, although occasional atrophy of some glomeruli and shrinking of renal corpuscles was observed
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