#6505 POST-BURNS PERSISTENT INFLAMMATION LEADS TO KIDNEY PROGRAMMED CELL DEATH THROUGH ACTIVATION OF THE CASPASES SIGNALING PATHWAY

Abstract Background and Aims The underlying mechanism for the increased incidence of chronic kidney disease (CKD) in burn patients discharged from hospital remains unclear. Recent studies have shown that are with inflammation despite normalization all physiological parameters. We hypothesized severe burns accelerate onset progression CKD by activating persistent inflammation. This study aimed to investigate long-term effects on its possible mechanisms. Method was divided into three parts. First, understand effect general population population, 4-month-old C57BL/6 mice were a blank control group (Blank) an adenine-induced group. Some established 10% total body surface area model at 5-month-old. Experiments terminated 7-month-old. function, morphology, inflammatory response oxidative stress assayed. Second, activated macrophages podocytes studied vitro experiments. Results In Blank group, did not cause function weight alterations, but caused small amount organic lesions, glomerular atrophy, apoptosis, macrophage infiltration. only significantly reduced also apoptosis addition, Caspase-1 -3 pathway expression mice. Electron microscopy showed aggravated injury including podocyte injury, cell membrane blubbing rupture. polarized M1 MPC5 death. Conclusion Severe programmed death through activation inflammation-induced Caspase-dependent pathways leading phenomenon has normal populations larger populations. important implications determining prognosis provides promising therapeutic strategy.