Oxidative stress does not contribute to the release of proinflammatory cytokines through activating the Nod-like receptor protein 3 inflammasome in patients with obstructive sleep apnoea.

Purpose: The study was conducted to test the hypothesis that oxidative stress leads to the release of proinflammatory cytokines by activating the Nod-like receptor protein (NLRP)3 inflammasome in patients with obstructive sleep apnoea (OSA).
Methods: The study recruited 247 participants who were divided into cases and healthy control groups. OSA patients were subdivided into four subgroups according to sex, blood pressure, body mass index (BMI), and severity of disease. No significant differences were found between cases and controls with respect to age or sex. Peripheral blood samples were collected for analysis after examination, and the serum concentrations of oxidative stress (8-isoprostane), inflammation (interleukin (IL)-18, IL-1β, IL-6, tumour necrosis factor (TNF)-α), and NLRP3 inflammasome components (NLRP3, caspase-1, and ASC) were detected by enzyme-linked immunosorbent assay.
Results: The serum concentrations of both oxidative stress and proinflammatory factors were higher in OSA patients than healthy controls. Subgroup analysis also revealed significant differences according to the apnoea-hypopnea index and BMI. Additionally, correlations were identified between 8-isoprostane and proinflammatory factors (IL-1β, IL-18, and TNF-α). Multiple regression analysis suggested that sleep parameters and BMI affected inflammation. However, no differences were observed in the serum level of NLRP3 inflammasome components between patients and controls. Furthermore, stratified analysis revealed no additional differences.
Conclusions: The current study suggests that oxidative stress leads to inflammation by mechanisms other than activation of the NLRP3 inflammasome in OSA patients. Furthermore, both sleep apnoea and BMI influenced the serum concentration of inflammatory mediators.