Long-term administration of advanced glycation end product stimulates the activation of NLRP3 inflammasome and sparking the development of renal injury

The accumulation of advanced glycation end products (AGE) and the enhanced interaction of AGE with their cellular receptor (RAGE) have been implicated in the progression of chronic kidney disease. The purpose of this study was to examine whether the AGE/RAGE-induced nephrotoxic effects are associated with inflammasome activation and endothelial dysfunction. Chronic renal injury was examined in BALB/c mice by the long-term administration of carbonyl-AGE for 16 weeks. Endothelial dysfunction was detected by measuring the number of circulating endothelial progenitor cells (EPCs) and the levels of nitric oxide synthase (eNOS) and nitric oxide (NO) in kidneys.

Source: The Journal of Nutritional Biochemistry - October 9, 2016 Category: Biochemistry Authors: Wan-Ju Yeh, Hsin-Yi Yang, Man-Hui Pai, Chi-Hao Wu, Jiun-Rong Chen Source Type: research