| Objective:To investigate whether hydrogen sulfide can reduce renal interstitial inflammatory response and further alleviate kidney damage by inhibiting Nod2 signaling pathway in renal ischemic reperfusion injury.Methods:Twenty-four male Wistar rats,weighting about 200 g,were randomly divided into 4 groups:Sham operation group(Sham);kidney ischemia reperfusion group(IRI);IRI + propargyl glycine(PAG)group(IRI+PAG);IRI + oxyammonia(HA)group(IRI+HA).The right kidney of Wistar rats were removed,Sham group separated the left kidney artery,24 hours later,extracted the kidney tissue samples;IRI Group subjected to occlusion of left kidney pedicle for 45 min,and then reperfusion,24 hours later extracted the kidney tissue samples.IRI+PAG group: which used left kidney artery intubation,injected PAG at a speed of 2 umol/ min,dosing for 20 min;IRI+HA group use the left renal artery intubation,injected HA at a speed of 300 nmol/L min,dosing for 20 min,the above two groups with IRI,we made the ischemic AKI model,extracted the kidney tissue samples.The protein levels of nucleotide combining oligomerization(Nod2)and nuclear NF-κB were analyzed by Western blotting.Expression of real-time quantitative PCR detected Nod2’s receptor mRNA.The protein levels of IL-1β expression was determined by immunohistochemical staining assay.Renal injuries were evaluated HE staining.Results:(1)Compared with the Sham group,in the IRI group,the Wistar rats kidney tissue Nod2,NF-κB,IL-1β protein expressions were increased significantly,the difference is statistically significant(P < 0.05);Nod2 mRNA expression increased significantly,the difference is statistically significant(P < 0.05);HE coloration showed the renal tubular epithelial cells swelled,withered,necrosised and blocked the lumen,a large number of inflammatory cells infiltrated in the renal interstitium,renal tubular interstitial injury score increased significantly,the difference is statistically significant(P < 0.05).(2)Compared with the IRI group,in the IRI+PAG and IRI+HA group Nod2,NF-κB,IL-1β protein expressions were upregulated significantly,the difference is statistically significant(P < 0.05);Nod2 mRNA expression were upregulated significantly,the difference is statistically significant(P < 0.05);HE coloration displayed acute tubular necrosis damage was aggravating,renal tubular interstitial injury score were upregulated significantly,the difference is statistically significant(P < 0.05).Conclusion:(1)In the case of renal ischemia reperfusion injury in Wistar rats,Nod2 signaling pathway is activated and can cause the renal tubular interstitial inflammatory response.(2)Inhibition of hydrogen sulfide,which further activating Nod2-like receptor dependent on inflammatory path,can increase renal ischemia reperfusion injury in ischemic acute kidney injury.(3)Hydrogen sulfide can inhibit the activation of Nod2 signaling pathway and reduce the inflammatory in ischemic reperfusion injury. |
