Evaluation of cell damage and allergy-induced mechanism by minute substance eluted from dental bio-materials

(1)随着镍离子浓度的增加，巨噬细胞样RAW264细胞活力下降，lps刺激的RAW264细胞一氧化氮生成也下降。DNA芯片分析显示，镍离子引起细胞周期阻滞、诱导细胞凋亡、炎症因子（IL-1α、IL-1α、IL-6、TNF）的产生和氧化应激的增加，从而导致细胞损伤和全身损伤，如过敏和癌症。(2)与不含钛离子的对照细胞相比，在含1ppm钛离子的培养基中培养的巨噬细胞样RAW264细胞存活率下降至55%左右。在含1ppm钛离子的培养基中培养的巨噬细胞样RAW264细胞的SOD活性和TNF-α产量比不含钛离子的对照细胞增加了一倍。推测巨噬细胞吞噬钛蛋白复合物引起炎症细胞反应。(3) 10μm钛颗粒在蒸馏水、MEM溶液和乳酸中洗脱15 d，分别为0、0.01 ppm和9 ppm，可忽略不计。吞噬10μm钛颗粒的巨噬细胞样RAW264细胞活力和NO生成量分别为89.4%和91.6%。这说明吞噬10μm钛颗粒对巨噬细胞造成的细胞损伤较小且可耐受。

(1)With increasing nickel ion concentrations, cell viability of macrophage-like RAW264 cells declined, and nitric oxide production of LPS-stimulated RAW 264 cells also declined. DNA microarray analyses showed that nickel ions caused cell cycle arrest, induction of apoptosis, production of inflammatory cytokines (IL-1α、IL-1α、IL-6、TNF) and increased oxidative stress, which lead to cellular damage and systematic body damage such as allergy and cancer.(2)Cell viability of macrophage-like RAW264 cells cultured in medium with 1ppm titanium ions declined to about 55%, compared to that of control cells without titanium ions. SOD activities and TNF-α production of macrophage-like RAW264 cells cultured in medium with 1ppm titanium ions doubled, compared to those of the control cells without titanium ions. It was speculated that phagocytosis of titanium-protein complex by macrophage caused inflammatory cellular reactions.(3)Elution of 10μm titanium particles into distilled water, MEM solution and lactic acid for 15 days was found to be negligible (0), 0.01 ppm and 9 ppm, respectively. Cell viability and NO production of macrophage-like RAW264 cells that phagocytized 10μm titanium particles were 89.4% and 91.6%, respectively. This means that macropage's cellular damage caisued by phagocytosis of 10μm titanium particles was small and tolerable.