Exogenous Hydrogen Sulfide Prevents SOD2 Degradation to Safeguard Renal Function in Diabetic Kidney Disease

This study was undertaken to unveil the mechanisms by which H2S counteracts against DKD. Utilizing mice and human renal tubular epithelial (HK-2) cells, we demonstrated a reduction in cystathionine-γ-lyase (CSE)/H2S levels within renal tissues of db/db mice and in HK-2 cells subjected to hyperglycemic and hyperlipidemic environments. Notably, we observed that NaHS supplementation could serve as an exogenous source of H2S. Exogenous H2S exhibited the capacity to mitigate the accumulation of reactive oxygen species (ROS) and attenuate the degradation of superoxide dismutase 2 (SOD2) by Lon protease homolog 1 (LONP1) induced by hyperglycemia and hyperlipidemia, thus affording cellular protection against mitochondrial apoptosis. Consequently, NaHS treatment led to decreased serum levels of blood urea nitrogen (BUN) and serum creatinine (SCr), reflecting alleviated renal damage and thereby preserving renal function in db/db mice. Based on these findings, we propose that exogenous H2S exerts a protective role against DKD by inhibiting SOD2 degradation.PMID:38417127 | DOI:10.1139/bcb-2023-0295
Source: Biochemistry and Cell Biology - Category: Biochemistry Authors: Source Type: research