HIF-1α特异性抑制剂YC-1对氯化钴诱导的巨噬细胞凋亡的影响  

Effect of HIF-1αSpecific Inhibitor YC-1 on Cobalt-chloride induced Macrophage Apoptosis

作　　者：胡娜[1] 肖靖杰 张爱梅[3] 李新芝[4] 魏丽丽[2] HU Na;XIAO Jing-jie;ZHANG Ai-mei;LI Xin-zhi;WEI Li-li(Medical teaching experimental center,Shihezi University School of Medicine,Xinjiang Shihezi,832002;Department of Physiology,Shihezi University School of Medicine,Xinjiang Shihezi,832002;Department of Cardiology,The First Affiliated Hospital of Shihezi University School of Medicine,Xinjiang Shihezi,832008;Department of Pathophysiology,Shihezi University School of Medicine,Xinjiang Shihezi,832002)

机构地区：[1]石河子大学医学院医学教学实验中心,新疆石河子832002 [2]石河子大学医学院生理学教研室,新疆石河子832002 [3]石河子大学医学院第一附属医院心内科,新疆石河子832008 [4]石河子大学医学院病理生理学教研室,新疆石河子832002

出　　处：《农垦医学》2020年第4期297-301,共5页Journal of Nongken Medicine

基　　金：国家自然科学基金(81860286)。

摘　　要：目的:研究低氧诱导因子1α(HIF-1α)特异性抑制剂YC-1对氯化钴(CoCl2)诱导的小鼠巨噬细胞损伤的保护作用及其分子机制。方法:以RAW264.7巨噬细胞为实验对象,CoCl2处理建立损伤模型,实验分为对照组、CoCl2处理组和YC-1预处理组。CCK-8法检测小鼠巨噬细胞活力;细胞凋亡检测试剂盒检测小鼠巨噬细胞凋亡比例;利用分光光度计法对丙二醛(MDA)含量进行检测;利用Western blot法完成HIF-1α表达水平的检测。结果:细胞损伤可在Co Cl2的作用下被诱导,而YC-1则能起到保护细胞的作用;YC-1增加了SOD活性、降低了MDA含量,YC-1能同时下调cleaved caspase-3及HIF-1α的表达水平。结论:YC-1能够显著改善CoCl2诱导的细胞损伤,且HIF-1α信号通路参与了YC-1对细胞的保护作用。Objective:To study the protective effect of HIF-1αspecific inhibitor yc-1 on cocl2-induced macrophage injury in mice and its molecular mechanism.Methods:Taking RAW264.7 macrophages as the experimental object,the damage model was established by CoCl2 treatment.macrophages were divided into control group,CoCl2 group and YC-1 pretreatment group.CoCl2 group was treated with 100 mumol/L CoCl2 intervention for 24 hours;YC-1 pretreatment group was treated with 10 mumol/L ycl1 pretreatment for 24 hours,and then 100 mumol/L CoCl2 intervention for 24 hours.Cell viability of each group was determined by CCK-8 method.Apoptosis detection kit was used to detect the apoptosis of mouse macrophages in each group.Spectrophotometer was used to detected the activity of superoxide dismutase(SOD)and malondialdehyde(MDA).Expression levels of cleaved caspase-3 and HIF-1αwere detected by Western blotting.Results:compared with CoCl2 group,YC-1 pretreatment could improve cell vitality,reduce apoptosis,increase SOD activity and reduce MDA content.Compared with the CoCl2 group,YC-1 could down-regulate the expression of cleaved caspase-3 and HIF-1α.Conclusion:YC-1 can significantly improve cocl2-induced cell damage,and theHIF-1αsignaling pathway participates in the protective effect of yc-1 on cells.

关 键 词：巨噬细胞 低氧诱导因子 低氧 细胞凋亡 

分 类 号：R329.25[医药卫生—人体解剖和组织胚胎学]