| First Author | Ma X | Year | 2013 |
| Journal | Arch Biochem Biophys | Volume | 533 |
| Issue | 1-2 | Pages | 1-10 |
| PubMed ID | 23500137 | Mgi Jnum | J:206702 |
| Mgi Id | MGI:5551704 | Doi | 10.1016/j.abb.2013.03.002 |
| Citation | Ma X, et al. (2013) Anti-inflammatory effects of propofol are mediated by apolipoprotein M in a hepatocyte nuclear factor-1alpha-dependent manner. Arch Biochem Biophys 533(1-2):1-10 |
| abstractText | Propofol (2,6-diisopropylphenol) is probably the most widely used intravenous hypnotic agent in daily practice. However, its anti-inflammatory properties have seldom been addressed. In this study, we evaluated the anti-inflammatory activity and mechanisms of propofol on lipopolysaccharide (LPS)-induced inflammation in vivo and in vitro and found that propofol markedly inhibited LPS-induced production of pro-inflammatory cytokines, including tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6, and expression of inducible nitric oxide synthase (iNOS). At the same time, the expression of hepatocyte nuclear factor-1alpha (HNF-1alpha) and apolipoprotein M (APOM) was inhibited by treatment with LPS and LPS-induced down-regulation of HNF-1alpha expression and APOM expression could be compensated by propofol treatment. However, propofol could not compensate LPS-induced down-regulation of APOM expression by treatment with HNF-1alpha siRNA and the suppressive effect on LPS-induced pro-inflammatory cytokines production by propofol was significantly compensated by treatment with APOM siRNA. These results provide evidence that propofol may first up-regulate APOM expression by enhancing HNF-1alpha expression and then inhibit pro-inflammatory cytokine production in LPS-stimulated cells. Therefore, our study may be useful in understanding the critical effect of propofol in patients with systemic inflammatory response syndrome. |
