The apoptosis of tubular epithelial cells in
diabetic nephropathy (DN) is commonly observed in human renal biopsies.
Inflammation plays a key role in DN, and
pentosan polysulfate (PPS) has been shown to largely attenuate the
inflammation of nephropathy in aging diabetic mice. p38 mitogen‑activated
protein kinase (p38 MAPK) plays a crucial role in tissue
inflammation and cell apoptosis, and it is activated by
hyperglycemia. In the present study, high glucose (HG)‑treated human renal proximal tubular epithelial cells (HK‑2) were used to examine the protective effects of PPS against HG‑stimulated apoptosis and
inflammation. The results of the study revealed that PPS markedly suppressed the HG‑induced reduction in cell viability. Incubation of HK‑2 cells with HG activated the
p38 MAPK pathway and, subsequently, as confirmed by western blot analysis and flow cytometry, increased cell apoptosis, which was blocked by PPS. In addition, PPS treatment significantly inhibited HG‑stimulated
p38 MAPK and nuclear factor‑κB activation, and reduced the production of pro‑inflammatory
cytokines, such as
tumor necrosis factor‑α,
interleukin (IL)‑1β and IL‑6. In conclusion, PPS ameliorates p38 MAPK‑mediated renal cell apoptosis and
inflammation. The anti‑apoptotic actions and anti‑inflammatory effects of PPS prompt further investigation of this compound as a promising therapeutic agent against DN.