Propofol inhibits the release of interleukin-6, 8 and tumor necrosis factor-α correlating with high-mobility group box 1 expression in lipopolysaccharides-stimulated RAW 264.7 cells

BACKGROUND: Studies have found that propofol can inhibit endotoxin-induced monocyte-macrophages to produce various inflammatory factors. This study is to disclose whether the propofol affects the expression of high-mobility group box 1 (HMGB1) in lipopolysaccharides (LPS)-stimulated RAW 264.7 cells and the release of interleukin-6 (IL-6), 8 (IL-8) and tumor necrosis factor-α (TNF-α). METHODS: RAW 264.7 cells were divided into four groups for intervention. After culturing for 16 h, the cells and culture supernatants were collected. The expression of HMGB1 in RAW 264.7 cells was detected by Western blot. The levels of IL-6, IL-8 and TNF-α in supernatants of cells were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: Stimulation of LPS increased the expression of HMGB1 and promoted the release of IL-6, IL-8 and TNF-α in supernatants of RAW 264.7 cells (p < 0.05); however, propofol down-regulated the expression of LPS-stimulated HMGB1 and reduced the LPS-stimulated releases of IL-6, IL-8 and TNF-α in supernatants of RAW 264.7 cells (p < 0.05). Moreover, the releases of IL-6, IL-8 and TNF-α intimately correlated with the expression of HMGB1 in this process (p < 0.05). CONCLUSION: Propofol inhibited the releases of IL-6, IL-8 and TNF-α in LPS-stimulated RAW 264.7 cells, and the levels of IL-6, IL-8 and TNF-α intimately correlated with the expression of HMGB1, which indicating that propofol may prevent inflammatory responses through reducing the releases of these cytokines and inflammatory mediators.