摘要
目的探讨动脉粥样硬化早期泡沫细胞形成与致炎症因子脂多糖(lipopolysaccharide,LPS)和抗炎因子白介素-10(interleukin-10,IL-10)的相互作用关系。方法以佛波醇酯(phorbol 12-myristate 13-acetate,PMA)诱导单核细胞株THP-1细胞分化为巨噬细胞,再以氧化型低密度脂蛋白刺激巨噬细胞形成泡沫细胞,采用油红O染色法同时观察致炎症因子LPS及抗炎因子IL-10在这一过程中对泡沫细胞形成的干预作用。结果氧化型低密度脂蛋白单独刺激巨噬细胞24 h后泡沫细胞的形成率由对照组的(9.77±1.70)%增加到刺激组的(16.27±2.27)%,且随时间延长增加更明显;LPS的协同作用能增加到40%以上,并随浓度升高而增多;IL-10能有效地抑制泡沫细胞形成,拮抗氧化型低密度脂蛋白和LPS的作用,且与浓度呈正相关。结论氧化型低密度脂蛋白能诱导泡沫细胞形成,LPS能明显加快泡沫细胞的转化,而抗炎因子IL-10能显著抑制这一过程。揭示血管炎症能加速泡沫细胞形成,而IL-10能抑制泡沫细胞的形成,这对延缓动脉粥样硬化进程具有重要作用。
Objective To study the effects of LPS and IL-10 on formation of foam cell during early atherosclerosis.Methods Macrophage was induced by PMA treatment of THP-1 cells,and then the cells were further stimulated by ox-LDL,ox-LDL plus LPS, ox-LDL plus IL-10 with or without LPS.By oil-red O staining technique,the formation of foam cells was evaluated by lipid granules formed in the cell.Results The proportion of foam cells formation was increased from（9.77±1.70）% to（16.27±2.27）% after 24 h stimulating with ox-LD,and the further increasing were observed with incubating time. The foam cells were significantly increased in the presence of LPS at a dose-dependem manner. The maximum increasing about 40 % was observed. However, the significant elevations by LPS were abrogated when IL-10 was added. These results indicated that IL-10 could effectively prevent the formation of foam cells induced by ox-LDL with or without LPS. Conclusion ox-LDL can cause foam cell formation from macrophage in vitro. LPS can significantly accelerate this event. Anti-inflammatory cytokine, IL-10 can inhibit the effect of LPS. These results indicate that inflammatory effects in blood vessels can speedup foam cell formation. The inhibition by IL-10 is very important for delaying atherosclerosis processes.
出处
《同济大学学报（医学版）》
CAS
2007年第1期1-5,9,共6页
Journal of Tongji University(Medical Science)
基金
国家自然科学基金资助项目(30671969)
