Figure 8.

Proposed scheme for the roles of SIRT1, p53, and other molecules in the protective effect of genistein on I/R-induced renal injury. Genistein treatment significantly reduced renal I/R-induced cell death, simultaneously stimulating renal cell proliferation. Paralleling the protective effect of genistein against I/R-induced renal injury, SIRT1 expression was upregulated upon the administration of genistein. Genistein reduced p53, p21, and cleaved caspase-3 expression and increased PCNA expression. Pharmacological inhibition or shRNA-mediated depletion of SIRT1 significantly reversed the effect of genistein on renal dysfunction, cellular damage, apoptosis, and proliferation following I/R injury. The reduced p53, p21 expression, and increased PCNA expression were blunted after the depletion of SIRT1 compared with the genistein treatment group in the renal I/R process.