To observe whether exogenous hydrogen sulfide (H₂S) donor sodium hydrosulfide (NaHS) can alleviate renal ischemia-reperfusion injury (IRI) in rats by inhibiting the expression of Toll-like receptor 2 (TLR2) and Toll-like receptor 4 (TLR4).

Twenty-four male SD rats aged 6-8 weeks were randomly divided into 3 groups: sham group (renal sham operation), I/R group (renal ischemia-reperfusion), and NaHS+ I/R group. Renal IRI was induced by right nephrectomy combined with left renal artery clipping for 45 minutes followed by 24 hours of reperfusion. Before the left renal artery clipping, the NaHS+ I/R group was given a continuous infusion of NaHS (300 nmol/min) for 10 minutes, while the sham group and I/R group were given an equal volume of normal saline. Abdominal aortic blood and kidney tissue samples were collected from each group. The expression of TLR2 and TLR4 protein in renal tissue was detected by western blotting. The expression of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in renal tissue was detected by immunohistochemistry. Blood urea nitrogen (BUN) and serum creatinine (Scr) were detected by colorimetry. HE staining was used to observe renal histological changes, and TUNEL method to detect renal tissue apoptosis.

Compared with the sham group, the I/R group showed more expression of TLR2, TLR4, IL-6 and TNF-α (P<0.05), higher levels of BUN and Scr (P<0.05), higher scores of the renal tubular injury (P<0.05), and more apoptotic cells in the renal tissue (P<0.05). Compared with the I/R group, the NaHS+ I/R group showed less expression of TLR2, TLR4, IL-6 and TNF-α (P<0.05), lower levels of BUN and Scr (P<0.05), lower scores of the renal tubular injury (P<0.05), and less apoptotic cells in the renal tissue (P<0.05).

Exogenous H₂S inhibited the expression of TLR2 and TLR4, reduced the release of inflammatory factors and apoptosis, and alleviated the renal IRI in rats.