Inhibition Of Oxidative Stress Alleviates Renal Ischemia-Reperfusion Injury Through The NOD1 Signaling Pathway

Objective:To investigate whether the inhibition of oxidative stress in renal ischemia-reperfusion injury(IRI)will reduce the kidney through the nucleotide binding oligodomain-like receptor 1(NOD1)signaling pathway Apoptosis and interstitial inflammation.Methods:Twenty-four male Wistar rats were randomly divided into 4 groups: the sham operation group: the right kidney was removed,and the left renal artery was isolated,and kidney tissue was collected for experiments after 24 hours;the kidney ischemia-reperfusion injury(IRI)group: After the left renal artery was isolated,the left renal pedicle was clamped for 45 min,and renal tissue was retained for experiment after 24 h of reperfusion;IRI + 4-hydroxy-3methoxyacetophenone(IRI +Apocynin)group: the intervention agent Apocynin The left renal artery was injected at a rate of 10 ?mol / min for 10 consecutive minutes.After the drug was discontinued for 3 minutes,the left renal pedicle of the rat was clamped with a microarterial clamp,and the block was released 45 minutes later to establish a rat acute renal ischemia-reperfusion model.Renal tissues were reserved for experiments;IRI +diiodobiphenyl chloride(IRI + DPI)group: the interventional agent DPI was injected at a rate of 1 ?mol / min for 10 minutes to the left renal artery,and 3 minutes after the drug was stopped,it was clamped with a microarterial clip The left renal pedicle was unblocked after 45 min.A rat model of acute renal ischemia-reperfusion was established,and kidney tissue was reserved for experiments.Both the Sham group andthe IRI group were injected with the same amount of saline as the intervention in the left renal artery.;Using Western blot to detect the expression of NOD1,Caspase-1,NF-?B in kidney tissue;The expression in renal tissue of an amount of the PCR method NOD1mRNA;HE staining to observe changes of pathology;immunohistochemical assay of TNF-? renal tissue;of TUNEL assay of apoptosis in renal tissues.Results:(1)Compared with the Sham group: the expression of NOD1,Caspase-1,NF-kB,and TNF-? protein in the kidney tissues of the IRI group was increased(all P <0.05);the expression of NOD1 mRNA was significantly increased(P <0.05);pathological tissues HE staining showed renal tubular epithelial cell edema,atrophy,necrosis,and renal tubular interstitial injury score increased(P <0.05);TUNEL staining showed an increase in the number of apoptotic cells in the ischemic area(P <0.05);(2)Compared with IRI group: The expression of NOD1,Caspase-1,NF-?B,TNF-? and other proteins in rat kidney tissues of IRI + Apocynin group and IRI + DPI group were significantly reduced(P <0.05);NOD1 mRNA expression was significant Decrease(P <0.05);Renal tubular necrosis was reduced and renal tubule interstitial injury score was significantly reduced by HE staining in pathological tissues(P <0.05);TUNEL staining showed a decrease in the number of apoptotic cells in ischemic area(P <0.05).Conclusion:(1)During ischemia-reperfusion injury of rat kidney tissue,NOD-1-NF-?B signaling pathway can be activated,which can aggravate renal cell apoptosis and interstitial inflammation.(2)Under the intervention of Apocynin / DPI,it can inhibit the activation of NOD-1-NF-?B signaling pathway and reduce renal cell apoptosis and interstitial inflammation.(3)Inhibition of oxidative stress in renal ischemia-reperfusion injury will reducerenal cell apoptosis and interstitial inflammation through the NOD1 signaling pathway.