Department of Cardiovascular Surgery, RenJi Hospital of Shanghai Jiaotong University, Shanghai, 200127, People's Republic of China.
Inflammation. 2012 Feb;35(1):342-9. doi: 10.1007/s10753-011-9324-6.
Nicotine has anti- and pro-inflammatory properties in various cells. Its role in aortic vascular smooth muscle cells (VSMC) was explored. Human aortic VSMC were cultured. After nicotine (1.0 μM) and/or pyrrolidinedithiocarbamic acid (PDTC, 50 μM) treatment, the activation of nuclear factor κB (NFκB) was investigated. The levels of pro-inflammatory cytokines, osteopontin (OPN), interleukin-6 (IL-6), and monocyte chemoattractant protein 1 (MCP-1) were also assessed. After OPN was downregulated by small interfering RNA (siRNA) transfection, the pro-inflammatory effect was reassessed. We found that NFκB was activated after nicotine administration. Nicotine upregulated OPN, IL-6, and MCP-1 expressions, and this effect attenuated after PDTC pretreatment. RNAi knocked down the OPN expression in nicotine-treated cells and abolished its pro-inflammatory effects. We concluded that nicotine induces a pro-inflammatory response in VSMC through a NFκB/osteopontin amplification loop-dependent pathway.
尼古丁在各种细胞中具有抗炎和促炎特性。本研究探讨了其在人主动脉血管平滑肌细胞（VSMC）中的作用。培养人主动脉 VSMC，用尼古丁（1.0 μM）和/或吡咯烷二硫代氨基甲酸盐（PDTC，50 μM）处理后，检测核因子 κB（NFκB）的激活情况。同时评估促炎细胞因子骨桥蛋白（OPN）、白细胞介素 6（IL-6）和单核细胞趋化蛋白 1（MCP-1）的水平。用小干扰 RNA（siRNA）转染下调 OPN 表达后，重新评估其促炎作用。结果发现，尼古丁处理后 NFκB 被激活。尼古丁上调 OPN、IL-6 和 MCP-1 的表达，而 PDTC 预处理则减弱了这种作用。RNAi 敲低了尼古丁处理细胞中的 OPN 表达，并消除了其促炎作用。综上所述，尼古丁通过 NFκB/骨桥蛋白放大环依赖性途径诱导 VSMC 发生促炎反应。
