BACKGROUND: The present study was conducted to explore the influence of remote ischemic preconditioning (RIPC) on the adjustment of renal fibrosis after ischemia-reperfusion injury (IRI).

MATERIAL AND METHODS: Male Sprague-Dawley rats were randomly assigned to 3 groups following right-side nephrectomy: the Sham group (without renal artery clamping), the IRI group (45 min left renal artery clamping), and the RIPC group (rats were treated daily with 3 cycles of 5 min of limb ischemia and 5 min of reperfusion on 3 consecutive days before left renal artery occlusion). After 3 months of reperfusion, the renal function and the extent of tubular injury and renal fibrosis were assessed. The expressions of transforming growth factor beta1 (TGF-β1), p-Smad2, Smad2, p-Smad3, and Smad3 were also evaluated.

RESULTS: There was no significant difference in renal function and tubular damage among the 3 groups after 45 min of kidney ischemia followed by 3 months of reperfusion. However, an obvious increase of extracellular matrix components and α-SMA could be observed in the kidney tissues of the IRI group, and the changes were significantly ameliorated in rats treated with enhanced RIPC. Compared with the IRI group, the expression of TGF-β1 and the level of p-Smad2 and p-Smad3 were decreased after the intervention of enhanced RIPC.

CONCLUSIONS: Enhanced RIPC ameliorated renal fibrosis after IRI in rats, which appears to be associated with inhibition of the TGF-β1/p-Smad2/3 signalling pathway.

Keywords: Fibrosis, Ischemic Preconditioning, Actins, Collagen Type I, Collagen Type III, Fibronectins, Kidney, Phosphorylation, Smad Proteins