Anti-inflammatory effects of propofol are mediated by apolipoprotein M in a hepatocyte nuclear factor-1α-dependent manner

作者：Ma, Xin; Hu, Yan-Wei; Zhao, Zhen-Long; Zheng, Lei; Qiu, Yu-Rong; Huang, Jin-Lan; Wu, Xiao-Juan; Mao, Xin-Ru; Yang, Jia; Zhao, Jia-Yi; Li, Shu-Fen; Gu, Miao-Ning^*; Wang, Qian

来源：Archives of Biochemistry and Biophysics, 2013, 533(1-2): 1-10.

DOI：10.1016/j.abb.2013.03.002

• Propofol
• LPS
• HNF-1 alpha
• APOM
• Inflammation

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)-1 beta, and IL-6, and expression of inducible nitric oxide synthase (iNOS). At the same time, the expression of hepatocyte nuclear factor-1 alpha (HNF-1 alpha) and apolipoprotein M (APOM) was inhibited by treatment with LPS and LPS-induced down-regulation of HNF-1 alpha 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-1 alpha 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-1 alpha 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.

• 出版日期2013-5
• 单位南方医科大学