Function of NLRP3 in the Pathogenesis and Development of Diabetic Nephropathy

Background: The aim of this research was to study the function of NLRP3 in the pathogenesis and development of diabetic nephropathy (DN). Material/Methods: We compared the expression of NLRP3-related protein in human glomerular mesangial cells under high glucose conditions at different times and in rats with DN of different ages. We also compared changes in IL-18 and IL-1 beta expression levels at different stages of DN. Results: After six hours, 12 hours, and 24 hours of high glucose stimulation, the secretion of IL-1 beta in human glomerular mesangial cells, compared to unstimulated cells, was 1.85-fold, 3.04-fold, and 4.14-fold; the expression of NLRP3 increased by 2.20-fold, 4.62-fold, and 8.32-fold; and the expression of caspase-1 was increased by 1.60-fold, 2.72-fold, and 3.67-fold. The expression levels of nephrin in eight-week-old and 12-week-old DN rats compared to 4-week rats were 49.60% and 21.20%, respectively. The IL-1 beta levels compared to four-week DN rats were 2.57-fold and 4.17-fold, respectively; NLRP3 levels were 1.29-fold and 2.17-fold respectively, and caspase-1 levels were 3.37-fold and 4.16-fold, respectively. The serum levels of IL-18 and IL-1 beta in the DN group were the highest at 218.53 +/- 30.69 pg/mL and 62.47 +/- 9.36 pg/mL, respectively; followed by the mild DN group at 177.07 +/- 32.88 pg/mL and 28.13 +/- 5.37 pg/mL, respectively, with the diabetic mellitus (DM) group having the lowest levels at 141.47 +/- 9.49 pg/mL and 15.53 +/- 3.26 pg/mL, respectively. The healthy control group levels were 99.40 +/- 22.72 pg/mL and 12.40 +/- 5.08 pg/mL, respectively. Conclusions: NLRP3 and high glucose activation may participate in the occurrence and development of DN by mediating the inflammatory response.