七氟醚可抑制氧化型低密度脂蛋白诱导巨噬细胞M1型极化  

Sevoflurane inhibits oxidized low-density lipoprotein-induced M1 polarization of macrophages

作　　者：徐国兴[1] 徐国亭[1] 李海中[1] XU Guoxing;XU Guoting;LI Haizhong(Department of Anesthesiology,First AffiliatedHospital of Henyang Medical College,Henyang 473003,China)

机构地区：[1]南阳医学高等专科学校第一附属医院麻醉科,473003

出　　处：《免疫学杂志》2021年第1期33-39,共7页Immunological Journal

摘　　要：目的探究七氟醚通过JAK3/STAT5信号通路对氧化型低密度脂蛋白(oxidized low-density lipoprotein,Ox-LDL)诱导巨噬细胞M1型极化的影响。方法酶联免疫法检测细胞培养液上清中肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-6(interleukin-6,IL-6)、转化生长因子-β(transforming growth factor-β,TGF-β)和白细胞介素-10(interleukin-10,IL^(-1)0)的水平,Westernblot检测诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)和精氨酸酶1(Arginase 1,Arg1)的表达。结果与对照组相比,Ox-LDL组巨噬细胞中i NOS蛋白的表达和培养液上清中TNF-α和IL-6的水平增加(P<0.05),而细胞中Arg1蛋白的表达水平和培养液上清中TGF-β和IL^(-1)0的水平降低(P<0.05),p-JAK3/JAK3和p-STAT5/STAT5的比值增加(P<0.05);与Ox-LDL组相比,Ox-LDL+Sevoflurane组的巨噬细胞中iNOS蛋白的表达和培养液上清中TNF-α和IL-6的水平降低(P<0.05),Arg1蛋白的表达水平和培养液上清中TGF-β和IL^(-1)0的水平升高(P<0.05),p-JAK3/JAK3和p-STAT5/STAT的比值降低(P<0.05);与Ox-LDL组相比,Ox-LDL+HY-P1061组巨噬细胞中iNOS蛋白的表达和培养液上清中TNF-α和IL-6的水平升高(P<0.05),Arg1蛋白的表达水平和培养液上清中TGF-β和IL^(-1)0的水平降低(P<0.05);与Ox-LDL+Sevoflurane组相比,Ox-LDL+Sevoflurane+HY-P1061组巨噬细胞中i NOS蛋白的表达和培养液上清中TNF-α和IL-6的水平升高(P<0.05),而细胞中Arg1蛋白的表达水平和培养液上清中TGF-β和IL^(-1)0的水平降低(P<0.05)。结论七氟醚抑制Ox-LDL诱导的巨噬细胞M1型极化,其机制可能与JAK3/STAT5信号通路的失活相关。This study was designed to investigate the effect of sevoflurane on oxidized low-density lipoprotein(Ox-LDL)-induced macrophage M1-type polarization through JAK3/STAT5 signaling pathway.Enzyme-linked immunosorbentassay(ELISA)was performed to detect the level of tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),transforming growth factor-β(TGF-β)and interleukin-10(IL^(-1)0)in the supernatant of cell culture;Western blot was used to detect the protein level of inducible nitric oxide synthase(iNOS)and arginase 1(Arg1).Compared with the control group,the Ox-LDL group demonstrated higher level of iNOS protein in macrophages,higher levels of TNF-αand IL-6 in the culture supernatant and higher ratio of p-JAK3/JAK3 and p-STAT5/STAT5,while lower level of Arg1 protein in macrophages and lower levels of TNF-αand IL-6 in the culture supernatant.Sevoflurane could reverse the changes mentioned above in the Ox-LDL group,while HY-P1061 could enhance the changes mentioned above in the Ox-LDL group.Compared with Ox-LDL+sevoflurane group,the OxLDL+sevoflurane+HY-P1061 group demonstrated higher level of iNOS protein in macrophages,higher levels of TNF-αand IL-6 in the culture supernatant and higher ratio of p-JAK3/JAK3 and p-STAT5/STAT5,while lower level of Arg1 protein in macrophages and lower levels of TNF-αand IL-6 in the culture supernatant.In conclusion,sevoflurane can inhibit Ox-LDL-induced macrophage M1 type polarization,and the mechanism may relate to the inactivation of JAK3/STAT5 signaling pathway.

关 键 词：OX-LDL 七氟醚 巨噬细胞 M1型极化 JAK3/STAT5信号通路 

分 类 号：R392.3[医药卫生—免疫学]