Renal ischemia/reperfusion (I/R) injury can lead to acute renal failure, delayed graft function and graft rejection. Nucleotide-binding oligomerization domain NOD-like receptor containing pyrin domain 3 (NLRP3)-mediated inflammation participates in the development of renal injury. Nrf2 accelerates NLRP3 signaling pathway activation and further regulates the inflammatory response. In addition, hydrogen sulfide serves a protective role in renal injury; however, the detailed underlying mechanism remains poorly understood. The present study investigated whether Nrf2 and NLRP3 pathway participate in hydrogen sulfide-regulated renal I/R-induced activation of the inflammatory response and apoptosis. Wild-type and Nrf2-knockout (KO) mice underwent surgery to induce renal I/R via clamping of the bilateral renal pedicles. A total of 20 mg/kg MCC950 (an NLRP3 inhibitor) was injected intraperitoneally daily for 14 days prior to surgery. Renal tissue and blood were collected from the I/R model mice to analyze NLRP3 and Nrf2 mRNA expression levels, NLRP3, PYD and CARD domain containing, caspase-1, IL-1β, Nrf2 and heme oxygenase 1 protein expression levels, cell apoptosis, the secretion of tumor necrosis factor-α, IL-1β and IL-6 cytokines and renal histopathology and function. Renal I/R activated the NLRP3 and Nrf2 signaling pathways. Conversely, MCC950 treatment inhibited activation of the NLRP3 signaling pathway, and prevented I/R-induced renal injury, release of cytokines and apoptosis in renal I/R model mice. Sodium hydrosulfide (NaHS) not only alleviated upregulation of NLRP3 protein expression levels, but also relieved renal injury, release of cytokines and cell apoptosis induced by renal I/R in wild-type mice, but not in Nrf2-KO mice. NaHS alleviated NLRP3 inflammasome activation, renal injury, the inflammatory response and cell apoptosis via the Nrf2 signaling pathway in renal I/R model mice.
In order to study the construction and application of urinary system model with functional bladder module, bladder model was designed, and appropriate materials was selected to make it, and its performance was studied. The results showed that in the analysis of pressure performance of bladder model, more detrusor instability was found in the model than in the urodynamic test, and there was significant statistical difference (P < 0.01). In the analysis of bladder safety capacity, it was found that the bladder safety capacity in the model was much larger than that measured by urodynamics, and there was significant statistical difference (P < 0.01). In the analysis of detrusor workmanship and contraction rate, it was found that the normal model group was significantly smaller than the obstruction group, and there was significant statistical difference (P < 0.01). Comparing the detrusor contraction rate of the two groups, it was found that the normal group and the obstruction group had significant difference at t3, and there was no statistical difference between the other two groups. Therefore, through this study, it is found that the understanding of urinary system can be enhanced by building bladder model, and the basic operating skills of medical staff can be improved more easily by using bladder model, which achieves the expected results of the experiment. Although some shortcomings have been found in the course of the study, it still provides experimental reference for the clinical study of bladder in the future.
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