麻黄碱对脂多糖诱导的小胶质细胞功能损伤的修复作用及机制OACSTPCD

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(75,150,300,600 μg/mL)on the viability and apoptosis of HMC3 cells.HMC3 cells were divided into control group(without drug intervention),LPS group(1 μg/mL),ephedrine group(1 μg/mL LPS+300 μg/mL ephedrine),BAY11-7082 group[1 μg/mL LPS+5 μmol/L nuclear factor-κB(NF-κB)pathway inhibitor BAY11-7082],inhibitor group(1 μg/mL LPS+300 μg/mL ephedrine+5 μmol/L BAY11-7082)and activator group(1 μg/mL LPS+300 μg/mL ephedrine+1 μmol/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 300 μg/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 associated with inhibiting the activity of the NF-κB signaling pathway.