摘要
目的研究麻黄碱对脂多糖(LPS)诱导的小胶质细胞功能损伤的修复作用及机制。方法以人小胶质细胞HMC3为研究对象,考察不同质量浓度麻黄碱(75、150、300、600μg/mL)对HMC3细胞活力和凋亡的影响。然后将HMC3细胞分为对照组(不受药物干预)、LPS组(1μg/mL)、麻黄碱组(1μg/mL LPS+300μg/mL麻黄碱)、BAY11-7082组[1μg/mL LPS+5μmol/L核因子κB(NF-κB)信号通路抑制剂BAY11-7082]、抑制剂组(1μg/mL LPS+300μg/mL麻黄碱+5μmol/L BAY11-7082)和激活剂组(1μg/mL LPS+300μg/mL麻黄碱+1μmol/L NF-κB信号通路激活剂Prostratin),加入相应药物作用24 h后,检测细胞迁移能力和细胞中可溶性白细胞介素6(sIL-6)、白细胞介素10(IL-10)、超氧化物歧化酶(SOD)、丙二醛(MDA)水平以及NF-κB信号通路相关蛋白表达水平。结果300μg/mL的麻黄碱可使HMC3细胞活力显著升高、凋亡率显著降低(P<0.05)。与对照组相比,LPS组迁移细胞数显著增多,细胞中sIL-6、MDA水平和NF-κB蛋白磷酸化水平均显著升高,IL-10、SOD水平均显著降低(P<0.05)。与LPS组相比,麻黄碱组和BAY11-7082组上述指标水平均显著逆转(P<0.05)。与麻黄碱组相比,抑制剂组迁移细胞数显著减少,细胞中sIL-6、MDA水平和NF-κB蛋白磷酸化水平均显著降低,IL-10、SOD水平均显著升高(P<0.05);而激活剂组上述指标水平均显著逆转(P<0.05)。结论麻黄碱可通过抑制LPS诱导的HMC3细胞凋亡、迁移、炎症和氧化应激,修复细胞功能损伤,其作用机制可能与抑制NF-κB信号通路活性有关。
OBJECTIVE To study the repair effect of ephedrine on lipopolysaccharide(LPS)-induced microglia function injury and its mechanism.METHODS Human microglia cells(HMC3)were used as research objects to investigate the effects of different concentrations of ephedrine(75,150,300,600μg/mL)on the viability and apoptosis of HMC3 cells.HMC3 cells were divided into control group(without drug intervention),LPS group(1μg/mL),ephedrine group(1μg/mL LPS+300μg/mL ephedrine),BAY11-7082 group[1μg/mL LPS+5μmol/L nuclear factor-κB(NF-κB)pathway inhibitor BAY11-7082],inhibitor group(1μg/mL LPS+300μg/mL ephedrine+5μmol/L BAY11-7082)and activator group(1μg/mL LPS+300μg/mL ephedrine+1μmol/L NF-κB pathway activator Prostratin).After 24 hours of drug treatment,cell migration,the levels of soluble interleukin-6(sIL-6),interleukin-10(IL-10),superoxide dismutase(SOD)and malondialdehyde(MDA),and the expressions of NF-κB pathway-related proteins were all detected.RESULTS The viability of HMC3 cells could be increased significantly by 300μg/mL ephedrine,while the apoptotic rate was decreased significantly(P<0.05).Compared with the control group,the number of migrating cells was increased significantly in the LPS group;the levels of sIL-6 and MDA,the phosphorylation of NF-κB protein were increased significantly,while the levels of IL-10 and SOD were decreased significantly(P<0.05).Compared with the LPS group,the above indexes were reversed significantly in the ephedrine group and BAY11-7082 group(P<0.05).Compared with the ephedrine group,the number of migrating cells was decreased significantly in the inhibitor group;the levels of sIL-6 and MDA,the phosphorylation of NF-κB protein were decreased significantly,while the levels of IL-10 and SOD were increased significantly(P<0.05).The above indexes were reversed significantly in the activator group(P<0.05).CONCLUSIONS Ephedrine can repair cell injury by inhibiting LPS induced apoptosis,migration,inflammation and oxidant stress of HMC3 cells,the mechanism of which may be associate
作者
尹涛
姜丽真
张盟盟
王睿健
张文超
YIN Tao;JIANG Lizhen;ZHANG Mengmeng;WANG Ruijian;ZHANG Wenchao(Dept.of Neurosurgery,Hengshui People’s Hospital(Harrison International Peace Hospital),Hebei Hengshui 053000,China;Dept.of Oncology,Hengshui People’s Hospital(Harrison International Peace Hospital),Hebei Hengshui 053000,China)
出处
《中国药房》
CAS
北大核心
2024年第1期33-37,共5页
China Pharmacy
基金
河北省科技计划重点研发项目(No.182777223)
衡水市科技计划项目(No.2022014083Z)。
关键词
小胶质细胞
麻黄碱
脂多糖
核因子ΚB信号通路
细胞功能损伤
microglia cells
ephedrine
lipopolysaccharide
nuclear factor-κB signaling pathway
cell function injury
