1,25(OH)(2)D-3 inhibits high glucose-induced apoptosis and ROS production in human peritoneal mesothelial cells via the MAPK/P38 pathway

摘要

The regulation of cell proliferation, differentiation and immunomodulation are affected by 1,25(OH)(2)D-3. However, its function during apoptosis and oxidative stress in human peritoneal mesothelial cells (HPMCs) remains unknown. The aim of the present study was to investigate whether the regulation of apoptosis and oxidative stress have therapeutic relevance in peritoneal dialysis (PD) therapy. The present study investigated the effects of 1,25(OH)(2)D-3 on high glucose (HG)-induced apoptosis and reactive oxygen species (ROS) production in HPMCs, and examined the underlying molecular mechanisms. Flow cytometry and western blotting were performed to detect cell apoptosis,2,7-dichlorofluorescein diacetate was used to measure reactive oxygen species production and 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide was used to measure cell viability. The results of the present study demonstrated that exposure to HG increased apoptosis and ROS production in HPMCs, whereas pretreatment with 1,25(OH)(2)D-3 significantly inhibited HG-induced apoptosis and ROS production. Further analysis revealed that 1,25(OH)(2)D-3 facilitated cell survival via the MAPK/P38 pathway. The results of the present study indicate that 1,25(OH)(2)D-3 inhibits apoptosis and ROS production in HG-induced HPMCs via inhibition of the MAPK/P38 pathway.