Abstract

Diabetic kidney disease is a frequent complication of diabetes and the predominant cause of end‑stage renal disease. However, the pathogenesis of diabetic kidney disease has not been fully elucidated. HK‑2 cells cultured in vitro were randomly divided into control, high glucose, high glucose + MCC950 and high glucose + irbesartan groups. The present study detected the mRNA and protein expression of NLRP3, caspase‑1, NF‑κB p65, α‑SMA, vimentin and N‑cadherin using reverse transcription‑quantitative PCR and western blotting. The present study also detected the protein expression of vimentin using immunocyte fluorescence. High glucose (40 mM) significantly increased the mRNA and protein levels of NLRP3, NF‑κB p65, caspase‑1 and epithelial‑mesenchymal transition (EMT) markers; these effects were attenuated by MCC950 and irbesartan administration. These results indicated that high glucose stimulation upregulated the expression of NLRP3 in HK‑2 cells and promoted the expression of EMT‑associated factors. Irbesartan inhibited the activation of the NLRP3 inflammasome and downregulated the expression of EMT‑related factors, which provided a basis for potential new strategies for the treatment of diabetic nephropathy.