摘要
目的探索硫化氢对THP-1源性巨噬细胞脂质摄取的影响及可能机制。方法采用荧光显微镜测DiI标记的氧化型低密度脂蛋白(DiI-ox-LDL)摄取、RT-PCR和免疫印迹法测定CD36 mRNA和蛋白表达。结果巨噬细胞与DiI-ox-LDL孵育后大量摄取氧化型低密度脂蛋白(ox-LDL),外源性硫化氢供体硫氢化钠显著抑制巨噬细胞摄取氧化型低密度脂蛋白,而炔丙基甘氨酸(一个硫化氢产生酶胱硫醚-γ-裂解酶抑制剂)加剧巨噬细胞摄取氧化型低密度脂蛋白。进而,硫氢化钠呈浓度依赖性抑制巨噬细胞CD36 mRNA和蛋白表达,而炔丙基甘氨酸促进巨噬细胞CD36 mRNA和蛋白表达。结论硫化氢抑制巨噬细胞摄取脂质及清道夫受体CD36表达。
Aim To investigate the effects of hydrogen sulfide(H2S) on ox-LDL uptake of THP-1-derived macrophages and its underlying mechanisms. Methods Fluorescence microscopy,RT-PCR and western blot were performed. Results Incubation of macrophages with DiI-ox-LDL led to ox-LDL uptake of macrophages.Sodium hydrosulfide(NaHS,an H2S donor) decreased ox-LDL uptake. While DL-propargylglgycine(PPG) exerted opposite effects.Furthermore,ox-LDL markedly induced CD36 mRNA and protein expression in macrophages,which was abolished by NaHS(50 to 100 μmol/L),but enhanced by PPG. Conclusions H2S inhibits ox-LDL uptake of THP-1-derived macrophages and down-regulates CD36 mRNA and protein expression.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2011年第2期85-88,共4页
Chinese Journal of Arteriosclerosis
基金
国家自然科学基金(30971169)
湖南省自然科学基金项目(09JJ6044)
湖南省科技计划项目(2008TP4038-2)
湖南省研究生创新项目(2008CXJJ04)
湖南省高校科技创新团队支持计划项目(2008-244)