Effect of xylitol on low‑density lipoprotein‑stimulated oxidative stress in THP‑1 cells.

Atherosclerosis (AS) is a chronic inflammatory disease caused by oxidative stress and the oxidation of low‑density lipoprotein (LDL). Xylitol, a widely used sugar substitute, has antioxidant potential; however, its effects on LDL‑induced oxidative stress in AS remain unclear. Using western blot, reverse transcription‑quantitative PCR, flow cytometry and so on, the present study investigated the role of xylitol in mitigating oxidative stress induced by high levels of LDL in Tohoku Hospital Pediatrics‑1 (THP‑1) human monocytic cell line), a model for studying AS. Xylitol significantly alleviated high LDL‑induced oxidative stress in THP‑1 cells and decreased reactive oxygen species levels, malondialdehyde content and the expression of NADPH oxidase family enzymes. Concurrently, xylitol enhanced the activity and expression of superoxide dismutase and increased the glutathione levels. Mechanistically, xylitol activated the nuclear factor erythroid 2‑related factor 2 (Nrf2)/heme oxygenase‑1 (HO‑1) axis by increasing the NADPH/NADP+ ratio via the regulation of the pentose phosphate pathway via the Nrf2 transcription factor. This led to a decrease in LDL oxidative modification in THP‑1 cells (Figs. 6,7). Overall, xylitol attenuates high LDL level‑induced oxidative stress in THP‑1 cells by modulating the Nrf2‑mediated pentose phosphate pathway and activating the Nrf2/HO‑1 axis, highlighting its potential for the prevention and treatment of AS.