Inflammatory responses induced by fluoride and arsenic at toxic concentration in rabbit aorta
Inflammatory responses induced by fluoride and arsenic at toxic concentration in rabbit aorta
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有毒浓度氟化物和砷引起的兔主动脉炎症反应
DOI：
10.1007/s00204-012-0803-9
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发表时间：
2012-06-01
影响因子：
6.1
通讯作者：
Wang, Jundong
中科院分区：
文献类型：
--
作者：
Ma, Yanqin;Niu, Ruiyan;Wang, Jundong
流行病学和实验研究已经证明了环境毒物砷和氟的致动脉粥样硬化作用。炎症机制在动脉粥样硬化的发病机制中起重要作用。本研究的目的是确定砷和氟单独或联合慢性暴露对兔主动脉炎症反应的影响。我们分析了参与白细胞粘附[P-选择素（P-sel）和血管细胞粘附分子-1（VCAM-1）]、白细胞募集和跨内皮迁移[白细胞介素-8（IL-8）和单核细胞趋化蛋白-1（MCP-1）]以及参与促炎细胞因子[白细胞介素-6（IL-6）]的基因的表达。我们发现，氟和砷单独或联合增加VCAM-1，P-sel，MCP-1，IL-8和IL-6在RNA和蛋白水平的表达。与仅暴露于其中一种相比，当同时暴露于两种毒物时，炎症相关分子的基因表达减弱。我们还检查了暴露于氟和（或）砷的家兔的血脂谱。结果表明，氟使血脂略有升高，砷使血清甘油三酯降低。我们发现，炎症反应而不是脂质代谢紊乱可能在砷和氟的心血管毒性机制中起着至关重要的作用。
Epidemiological and experimental studies have demonstrated the atherogenic effects of environmental toxicant arsenic and fluoride. Inflammatory mechanism plays an important role in the pathogenesis of atherosclerosis. The aim of the present study is to determine the effect of chronic exposure to arsenic and fluoride alone or combined on inflammatory response in rabbit aorta. We analyzed the expression of genes involved in leukocyte adhesion [P-selectin (P-sel) and vascular cell adhesion molecule-1(VCAM-1)], recruitment and transendothelial migration of leukocyte [interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1)] and those involved in pro-inflammatory cytokines [interleukin-6 (IL-6)]. We found that fluoride and arsenic alone or combined increased the expression of VCAM-1, P-sel, MCP-1, IL-8, and IL-6 at the RNA and protein levels. The gene expressions of inflammatory-related molecules were attenuated when co-exposure to the two toxicants compared with just one of them. We also examined the lipid profile of rabbits exposed to fluoride and (or) arsenic. The results showed that fluoride slightly increased the serum lipids but arsenic decreased serum triglyceride. We showed that inflammatory responses but not lipid metabolic disorder may play a crucial role in the mechanism of the cardiovascular toxicity of arsenic and fluoride.