Renoprotective mechanisms of celastrol in high glucose-mediated HK-2 cell injury through inhibition of the PI3K/Akt/NF-κB signalling pathway.

ABSTRACT: Hyperglycemia-induced inflammation and fibrosis in renal tubular epithelial cells are critical factors driving the progression of diabetic nephropathy (DN). Celastrol, a bioactive compound derived from Tripterygium wilfordii Hook.F, is recognized for its anti-inflammatory and anti-fibrotic properties. This study aimed to investigate the renoprotective effects of celastrol against high glucose (HG)-induced damage in human kidney 2 (HK-2) cells. Briefly, HK-2 cells were exposed to high glucose and treated with celastrol. Cell viability and apoptosis were evaluated using CCK-8 assay kit and flow cytometry, respectively. The pro-inflammatory cytokines, oxidative stress markers, and fibrotic-related proteins were measured using ELISA and immunoblotting. To further confirm the mechanistic

SUBMITTER: Wang X 

PROVIDER: S-EPMC11803244 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature