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

Abstract 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

The Schistosoma japonicum genome reveals features of host–parasite interplay

Schistosoma japonicum is a parasitic flatworm that causes human schistosomiasis, which is a significant cause of morbidity in China and the Philippines. Here we present a draft genomic sequence for the worm. The genome provides a global insight into the molecular architecture and host interaction of this complex metazoan pathogen, revealing that it can exploit host nutrients, neuroendocrine hormones and signalling pathways for growth, development and maturation. Having a complex nervous system and a well-developed sensory system, S. japonicum can accept stimulation of the corresponding ligands as a physiological response to different environments, such as fresh water or the tissues of its intermediate and mammalian hosts. Numerous proteases, including cercarial elastase, are implicated in mammalian skin penetration and haemoglobin\ud degradation. The genomic information will serve as a valuable platform to facilitate development of new interventions for schistosomiasis control