Abstract

Cisplatin is used as a potent anticancer drug, but it often causes nephrotoxicity. Bee venom (BV) has been used for the treatment of various inflammatory diseases, and its renoprotective action was shown in NZB/W mice. However, little is known about whether BV has beneficial effects on cisplatin-induced nephrotoxicity and how such effects might be mediated. In the present study, the BV-injected group showed a significant increase in the population of Tregs in spleen. Although there was no significant difference in the numbers of Tregs 3 days after cisplatin injection between the BV- and PBS-injected groups, more migration of Tregs into the kidney was observed 6 hours after cisplatin administration in BV group than in PBS group. In addition, BV-injected mice showed reduced levels of serum creatinine, blood urea nitrogen, renal tissue damage, proinflammatory cytokines, and macrophage infiltration into the kidney 3 days after cisplatin administration. These renoprotective effects were abolished by the depletion of Tregs. The anticancer effect of repeated administrations of cisplatin was not affected by BV injection. These results suggest that BV has protective effects on cisplatin-induced nephrotoxicity in mice, at least in part, through the regulation of Tregs without a big influence on the antitumor effects of cisplatin. © 2013 Hyunseong Kim et al.

Indexed keywords

EMTREE drug terms: bee venom; cisplatin; creatinine; cytokine; protective agent; transcription factor FOXP3

EMTREE medical terms: animal cell; animal experiment; animal tissue; article; CD4+ CD25+ T lymphocyte; cell infiltration; cell migration; controlled study; creatinine blood level; kidney injury; macrophage; male; mouse; nephrotoxicity; nonhuman; priority journal; regulatory T lymphocyte; renal protection; urea nitrogen blood level

Chemicals and CAS Registry Numbers: cisplatin, 15663-27-1, 26035-31-4, 96081-74-2; creatinine, 19230-81-0, 60-27-5