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目的:探讨Sirt1在内质网应激诱导巨噬细胞凋亡中的作用。方法:用衣霉素、白藜芦醇、尼克酰胺干预巨噬细胞后,应用Western blot检测Sirt1、内质网应激标志物GRP78、CHOP的活性,应用流式细胞仪检测巨噬细胞凋亡。结果:衣霉素诱发了巨噬细胞内质网应激,GRP78、CHOP以及细胞凋亡明显高于对照组(P<0.05),同时激活了Sirt1,与对照组相比P<0.05;应用衣霉素干预巨噬细胞同时,加用Sirt1激活剂白藜芦醇,与单用衣霉素组相比,Sirt1明显增高(P<0.05),GRP78、CHOP以及细胞凋亡明显减少(P<0.05);应用衣霉素干预巨噬细胞同时,加用Sirt1抑制剂尼克酰胺,与单用衣霉素组相比,Sirt1明显减少(P<0.05),GRP78、CHOP以及细胞凋亡明显增加(P<0.05)。结论:Sirt1可以保护内质网应激诱导的巨噬细胞凋亡。
Objective: To investigate the role of Sirt1 in endoplasmic reticulum stress-induced apoptosis of macrophages. METHODS: Macrophages were treated with tunicamycin, resveratrol and nicotinamide. Western blot was used to detect the activity of Sirt1 and endoplasmic reticulum stress markers GRP78 and CHOP. The apoptosis of macrophages was detected by flow cytometry . Results: Tunicamycin induced endoplasmic reticulum stress, GRP78, CHOP and apoptosis in macrophages were significantly higher than the control group (P <0.05), Sirt1 activated at the same time, P <0.05 compared with the control group; At the same time, the addition of Sirt1 activator, resveratrol, significantly increased Sirt1 (P <0.05) and decreased GRP78, CHOP and apoptosis in macrophages compared with those treated with tunicamycin alone (P <0.05 (P <0.05), GRP78, CHOP and apoptosis were significantly increased (P <0.05). The application of tunicamycin to macrophages also increased Sirt1 inhibitor nicotinamide compared with single tunicamycin group <0.05). Conclusion: Sirt1 can protect endoplasmic reticulum stress-induced apoptosis of macrophages.