Objective   To investigate the effect of hydrogen sulfide on renal function in rats with acute kidney injury induced by sepsis.

  Methods   A model of sepsis-induced acute kidney injury in male Sprague-Dawley (SD) rats was established with cecal ligation and puncture. Totally 120 male SD rats were randomly divided into a control group (with sham operation), a model group and low-, moderate-, and high- hydrogen sulfide treatment group (20, 50, 100 μmol/L). The rats′ renal function, inflammatory response, histological changes, apoptosis and fibrosis in renal tissues were observed. Western blot was used to detect cleaved caspase-3, cleaved caspase-9, B-cellymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax), transforming growth factor β (TGF-β), fibronectin, and α-smooth muscle actin (α-SMA) in renal tissues. Serum inducible nitric oxide synthase (iNOS), interleukin 6 (IL-6), and interleukin 10 (IL-10) were detected with enzyme-linked immunosorbent assay (ELISA).

  Results  In the model rats, renal cell necrosis and exfoliation, glomerular capillary congestion/edema/vacuolar degeneration, and narrowing of renal tubular lumen were observed and compared with those in the control rats, urinary protein, urea nitrogen and creatinine increased significantly (P < 0.05 for all); cleaved caspase-3, cleaved caspase-9, the ratio of Bax/Bcl-2, TGF-β, fibronectin, and α-SMA in kidney tissues were significantly up-regulated. In the rats treated with hydrogen sulfide, significantly reduced urinary protein and urea nitrogen/creatinine, down-regulated iNOS and IL-6 but up-regulated anti-inflammatory factor IL-10, significantly down-regulated apoptosis-related cleaved caspase-3, cleaved caspase-9, and Bax/Bcl-2, fibrosis-related TGF-β, fibronectin, and α-SMA were detected in comparison with the model rats.

  Conclusion  Hydrogen sulfide could inhibit inflammatory response, apoptosis and renal fibrosis in rats with acute kidney injury induced by sepsis.