Sirt1抑制内质网依赖的巨噬细胞凋亡

Sirt1 inhibits endoplasmic reticulum dependent macrophage apoptosis

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 the apoptosis of macrophage induced by endoplasmic reticulum stress. Methods： After macrophage treated with tunicamycin,resveratrol and nicotinamide,Sirt1,endoplasmic reticulum stress markers GRP78 and CHOP were detected usingh Western blot,the apoptosis of macrophage was tested by flow cytometry. Results： The tunicamycin induced macrophage endoplasmic reticulum stress.GRP78,CHOP and apoptosis in the group treated with tunicamycin were significantly higher than those in the control group（ P 0. 05）,and Sirt1 was activated at the same time compared with the control group（ P 0. 05）. When treated with bothtunicamycin and Sirt1 activator resveratrol,GRP78,CHOP and apoptosis were significantly decreased（ P 0. 05）,and Sirt1 was significantly increased（ P 0. 05） compared with the single tunicamycin group.Sirt1 decreased significantly（ P 0. 05）,GRP78,CHOP and cells apoptosis were significantly increased（ P 0. 05） when treated with bothtunicamycin and Sirt1 inhibitor nicotinamide. Conclusion： Sirt1 can protect endoplasmic reticulum stress-induced apoptosis of macrophages.