Key result
Proanthocyanidin dose-dependently reverses cisplatin-induced renal toxicity and oxidative stress in mice.
Why the study?
Does proanthocyanidin attenuate cisplatin-induced oxidative renal toxicity in mice?
Does proanthocyanidin attenuate cisplatin-induced oxidative renal toxicity in mice?
Proanthocyanidin shows potential in attenuating cisplatin-induced oxidative renal toxicity in a mouse model.
PA attenuates CP nephrotoxicity in mice; hypothesis-generating for renoprotection during chemotherapy, with human trials required.
Cisplatin (CP) [cis-diamminedichloroplatinum (II)] is one of the most widely therapeutic agents used for treating many types of cancer. At effective doses, CP causes nephrotoxicity which has been attributed to the induction of reactive oxygen species (ROS). In the present investigation proanthocyanidin (PA) was studied to demonstrate its therapeutic efficacy against CP-induced nephrotoxicity in mice. Cp treatment caused significant elevation of urea, creatinine and IL-6. In addition, CP enhanced malondialdehyde (MDA) levels and lowered the glutathione (GSH) content in kidney. On the other hand, superoxide dismutase (SOD) activity was decreased. These alterations were reversed by PA in a dose-dependent manner. These findings suggested a beneficial role of PA in attenuating CP-induced oxidative renal toxicity.
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Ahmed Amir Radwan Sayed (2009) studied Cisplatin-induced nephrotoxicity. Proanthocyanidin vs. Cisplatin alone was evaluated on Renal toxicity markers (urea, creatinine, IL-6, MDA, GSH, SOD). Proanthocyanidin reversed cisplatin-induced elevations in urea, creatinine, IL-6, and MDA, and restored GSH and SOD levels in a dose-dependent manner in mice.
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