Propofol attenuates intermittent hypoxia induced up-regulation of proinflammatory cytokines in microglia through inhibiting the activation of NF-Bκ/p38 MAPK signalling.

<i>As immune sentinels of the central nervous system (CNS), microglia is pivotal cellular mediator of neuroinflammatory processes. Activation of microglia might elicit the expression of proinflammatory cytokines involved in the progression of neuroinflammatory diseases. Numerous studies have demonstrated that propofol (2,6-diisopropylphenol) has an effective anti-inflammatory property. Intermittent hypoxia (IH), as a result of obstructive sleep apnoea (OSA), could lead to neuron damage and neuroinflammation in the CNS. Here, we determined the effects of propofol on the inflammatory response in microglia during IH. The levels of nuclear factor-Bκ (NF-κB) inhibitor (IκB) and activated p38 mitogen-activated protein kinase (MAPK) exposed to IH with or without propofol treatment were detected by Western blot. The viability of cells exposed to various concentrations of propofol was monitored with MTT assay. The production and mRNA levels of tumor necrosis factor- α(TNF-α) and interleukin-6 (IL-6) were evaluated by qRT-PCR and ELISA, respectively. As results, IH exposure obviously promoted the activation of NF-κB/p38 MAPK signalling and the secretion of TNF-α and IL-6. Propofol was not toxic to microglia. Compared with the control group, propofol attenuated the IH-induced activation of NF-Bκ and p38 MAPK, which accompanied with reduction of proinflammatory cytokine secretion. These data suggested that propofol down-regulated the IH-induced secretion of proinflammatory cytokine, and inhibit inflammatory responses in microglia, and might be involved in attenuation of the p38 MAPK and NF-κB signalling pathways. Overall, propofol could contribute to alleviating IH-induced CNS diseases in patients by inhibiting p38 MAPK and NF-κB mediated inflammation in microglia.</i>.