Objective To investigate the effect of low-dose cyclosporine A （CsA）on mitochondrial permeability transition of tubular cells induced by ischemic acute renal failure (ARF) in a rat model. Methods Male Wistar rats were divided randomly into 3 groups (sham, ARF and ARF+CsA). ARF was induced by clamping both renal arteries for 30 min. The animals were pretreated with vehicle or CsA intraperitoneally 15 min before ischemia, and were sacrificed at 18 h of reperfusion. Renal function following ARF was determined by measur-ing serum creatinine. Tubular cell apoptosis was confirmed by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) assay. Protein expressions of renal cytosolic cytochrome c, caspase-3, 9 were analyzed by Western blot analysis. Results Serum creatinine levels significantly increased after acute renal injury［(106.9±19.4)μmol/L vs (56.5±7.1)μmol/L，P＜0.05]. Renal ischemia injury induced a significant increase of apoptotic tubular cells [(20.14±3.70)% vs (0.99±0.17)%，P＜0.05]. Protein expressions of cytosolic cytochrome c, caspase-3, 9 in the kidneys of ARF group were markedly up-regulated (P＜0.05). CsA significantly improved renal function［(87.5±18.5)μmol/L］, reduced apoptotic tubular cells and inhibited the up-regulation of cytosolic cytochrome c, caspase-3, 9 expressions (P＜0.05). Conclusions Low-dose CsA inhibits mitochondrial permeability transition of tubular cells in ischemic ARF, which may essentially contribute to its anti-apoptotic effects.