The Nephron journals/Nephron journals · 1999 · 29 citations · 24 references
MedicineNephrologyPharmacologyBiochemical PharmacologyRenal PathophysiologyRenal PharmacotherapyNephrotoxicity MechanismsRenal DiseaseRenal PharmacologyRenal ToxicityBlood Urea Nitrogen To Creatinine RatioMalondialdehyde FormationProximal Tubule PhysiologyRenal Antioxidant DefenseRenal Oxidative StressRenal Tissue InjurySuperoxide Dismutase FunctionUrinary Urea Nitrogen
To determine whether ginsenoside-Rd ameliorates the renal injury induced by cephaloridine, the effect of cephaloridine was investigated in rats given ginsenoside-Rd preceding cephaloridine administration and in control rats given no ginsenoside-Rd. In control rats, blood, renal and urinary parameters and the activities of antioxidative enzymes in renal tissue deviated from the normal range, indicating dysfunction of the kidneys. In contrast, when ginsenoside-Rd was given orally for 30 consecutive days prior to cephaloridine injection, the activities of the antioxidation enzymes superoxide dismutase and catalase were higher, while malondialdehyde levels in serum and renal tissue were lower in the treated rats than in the controls. The urea nitrogen and creatinine levels in serum were decreased in rats given ginsenoside-Rd. Decreased urine volume, increased urinary osmotic pressure, and decreased urinary levels of glucose, protein, sodium and potassium demonstrated a protective action against the renal dysfunction caused by cephaloridine. In addition, it was demonstrated that ginsenoside-Rd affected cultured proximal tubule cells exposed to cephaloridine.
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