Albumin evokes Ca 2+ -induced cell oxidative stress and apoptosis through TRPM2 channel in renal collecting duct cells reduced by curcumin

摘要: In proteinuric nephropathies of chronic kidney disease, the epithelial cells nephron including collecting duct are exposed to high concentrations luminal albumin. Albumin is taken up from by endocytosis causing excessive reactive oxygen species (ROS) production and a proinflammatory response. Curcumin used in traditional medicine possesses anti-inflammatory antioxidant effects. ROS ADP-ribose (ADPR) activate cation channel TRPM2. We hypothesize, that albumin-induced cell stress response mediated Ca2+ can be reduced curcumin. The cortical (CCD) mpkCCDc14 exhibit spontaneous inducible oscillations, which blocked pre-treatment with accumulates plasma membrane intracellular vesicles, where it interferes TRPM2 decreases influx Ca2+. reduces viability increases apoptosis, NF-κB activation, mitochondrial depolarization via Ca2+-dependent signaling, results increased production. Albumin-induced diminished inhibition after administration curcumin ADPR (PARP1) inhibitors. did not reduce elevation induced thapsigargin Ca2+-free medium, but function store-operated channels ATP-evoked response. In conclusion, oxidative signaling leads damage response, strengthening role CCD progression disease.