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二氧化硅引起巨噬细胞形态学变化和肿瘤坏死因子的表达 被引量:2

SILICON DIOXIDE INDUCED MORPHOLOGICA CHANGES AND TNF-α EXPRESSION IN MOUSE RAW264.7 MACROPHAGES
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摘要 目的:研究不同浓度二氧化硅(SiO2)是否诱导培养的小鼠巨噬细胞RAW264.7的形态学变化和肿瘤坏死因子-α(TNF-α)的表达。方法:用不同浓度的SiO2刺激巨噬细胞后,观察其细胞的形态学改变,并用免疫细胞化学检测其TNF-α的蛋白表达。结果:与对照组相比SiO2浓度为25μg/mL时,巨噬细胞形态和TNF-α蛋白表达无明显改变(F=229.99,P>0.05);随着SiO2浓度的增加(50~100μg/mL)巨噬细胞外形略显不规则,但仍不明显,而TNF-α蛋白表达则明显增加(P<0.01);当SiO2浓度为150μg/mL时,细胞形态改变明显,表现为细胞突起变长,数量明显减少,胞质内颗粒增多,部分细胞开始崩解,且TNF-α蛋白表达亦明显增加(P<0.01)。结论:巨噬细胞分泌的TNF-α在硅肺的发生中可能起重要作用。 Objective: To study whether silicon dioxide at different concentrations induces morphological changes and TNF-α expession in cultured mouse RAW264.7 macrophages. Methods: After stimulation with different concentrations of silicon dioxide, the morphological changes of the above macrophages were observed and the TNF-α expression was detected by immunocytochemistry as well.Results:There were no morphological changes and increase of TNF-α expression in the cultured macrophages treated with 25 μg/mL silicon dioxide, as compared with the control group(F=229.99,P > 0.05). With the increased silicon dioxide concentrations(from 50 μg/mL to 100 μg/mL), there were still no significant morphological changes to be found although the cellular outlines became mild irregular,whereas the TNF-α protein expression in the cells was significantly increased(P < 0.01). After treatment with silicon dioxide at a concentration of 150 μg/mL,the morphological changes of cells became significant which showed prolongation of the cell processes and decrease of the cell number,increased granules in the cytoplasm,part destruction of the cells initially,and the TNF-α protein expression was also increased(P < 0.01(. Conclusion: The increased TNF-α production bymacrophages might play an important role in the pathogenesis of silicosis.
出处 《海南医学院学报》 CAS 2005年第1期12-14,共3页 Journal of Hainan Medical University
基金 海南省自然科学基金资助项目(80438) 海南医学院苗圃基金资助项目(200304)
关键词 巨噬细胞 蛋白表达 TNF-α 形态学变化 改变 肿瘤坏死因子 RAW264.7 SIO2 二氧化硅 并用 Macrophages Tumor necrosis factor-alpha Silicon dioxide
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