| Objective:To observe whether exogenous hydrogen sulfide(H2S)donor sodium hydrosulfide(NaHS)can alleviate renal ischemia-reperfusion injury(IRI)in rats by inhibiting the activation of Toll-like receptor 2(TLR2)and Toll-like receptor 4(TLR4).Methods: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.After 10%chloral hydrate anesthesia(0.3ml/100g),the rats were fixed to an anatomical plate,cut open the abdominal cavity,passively separated the tissue around the pedicle,ligated the right pedicle and had the right kidney removed.The left renal artery was intubated,and 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.After 5 minutes’suspension,the Sham group was not clamped,while the other two groups were treated with a non-invasive microarterial clamp after 45 minutes’closure of the left renal artery,and then the occlusion was released to establish acute kidney I/R models.After 24 hours,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.Results: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 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).Conclusion:1.Under the condition of renal ischemia-reperfusion in rats,the expression of TLR2and TLR4 protein increased,which aggravated renal injury by promoting inflammatory response and apoptosis.2.Exogenous H2S inhibited the expression of TLR2 and TLR4,reduced the release of inflammatory factors and apoptosis,and alleviated the renal IRI in rats. |