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目的探讨超声介导携氧载紫杉醇脂质微泡对乏氧巨噬细胞增殖和凋亡的影响。方法筛选超声辐照小鼠巨噬细胞RAW264.7合适的超声参数,用Co Cl2诱导小鼠巨噬细胞RAW264.7乏氧模型,将乏氧巨噬细胞随机分为对照组(controlgroup)、紫杉醇组(PTX group)、甲氨蝶呤组(MTX group)、超声组(US group)、携氧脂质微泡组(OMBs group)、携氧载紫杉醇脂质微泡组(OPLMBs group)和超声介导携氧载紫杉醇脂质微泡组(OPLMBs+US group),分别进行干预。采用MTT法检测各处理组巨噬细胞增殖,Annexin V-FITC/PI双染法检测各组细胞凋亡。结果超声强度为0.5 W/cm2,连续作用30 s时细胞存活率为(95.85±2.36)%。超声介导携氧载紫杉醇脂质微泡组增殖抑制率及凋亡率分别为(46.01±2.35)%和(27.64±1.36)%,明显高于其它各处理组(P<0.05)。结论超声介导携氧载紫杉醇脂质微泡能明显抑制乏氧巨噬细胞的增殖、诱导其凋亡,可为RA体内实验研究提供思路。
Objective To investigate the effects of ultrasound-mediated paclitaxel-loaded lipid microbubbles on proliferation and apoptosis of hypoxic macrophages. Methods The ultrasound parameters of RAW264.7 macrophages were sonicated by ultrasound. CoCl2 was used to induce macrophage RAW264.7 hypoxia. The hypoxic macrophages were randomly divided into control group, paclitaxel PTX group, MTX group, US group, OMBs group, OPLMBs group and ultrasonography Mediated oxygen-carrying paclitaxel lipid microbubbles group (OPLMBs + US group), respectively, for intervention. The proliferation of macrophages in each treatment group was detected by MTT assay. The apoptosis of each group was detected by Annexin V-FITC / PI double staining. Results The ultrasound intensity was 0.5 W / cm2. The cell survival rate was (95.85 ± 2.36)% at 30 s. Ultrasound-mediated paclitaxel-loaded liposome-containing microbubbles group proliferation inhibition rate and apoptosis rate were (46.01 ± 2.35)% and (27.64 ± 1.36)%, significantly higher than the other treatment groups (P <0.05). Conclusion Ultrasound-mediated paclitaxel-loaded lipid microbubbles can significantly inhibit the proliferation of hypoxic macrophages and induce their apoptosis, which may provide a new idea for the experimental study in RA.