石杉碱甲保护人脑微血管内皮细胞损伤的体外实验研究

Protect Effects of Huperzine A on Methylglyoxal Induced Injury in the Cultured Human Brain Microvascular Endothelial Cell in Vitro Experimental Study

目的体外实验研究石杉碱甲对人脑微血管内皮细胞(human brain microvascular endothelial cells,HBMEC)损伤的保护作用和机制。方法在培养的HBMEC上,利用丙酮醛诱导细胞损伤,通过MTT检测细胞活力,LDH、SOD活性试剂盒及caspase-3活性试剂盒检测细胞损伤情况,观察石杉碱甲的作用和机制。结果石杉碱甲呈浓度依赖地保护MGO诱导的细胞损伤,在10-5mol·L-1时呈最大保护作用。丙酮醛能诱导HBMEC的SOD活性下降,而石杉碱甲(10-6,10-5mol·L-1)能逆转这种作用。进一步研究发现石杉碱甲能抑制丙酮醛诱导的caspase-3活性上升。结论石杉碱甲对丙酮醛诱导的HBMEC的损伤具有保护作用,这可能与其抗自由基和抗凋亡作用有关。

OBJECTIVE To evaluate the effects ofhuperzine A on the methylglyoxal（MGO） induced injury in the culturedhuman brain microvascular endothelial cell（HBMEC）.METHODS HBMEC cell line was chosen to induce MGO injury.Cell vitality was measured by using MTT,LDH release,SOD activity were tested by kits.Cell apoptosis was measured by caspase 3 activity.RESULTS Huperzine A dose-dependently protected MGO induced HBMEC injury.At 10-5mol·L-1 ofhuperzine A manifested the maximum effects.MGO increased SOD activity,which were reversed by pretreatment of venlafaxine（10-6 and 10-5mol·L-1）.Furthermore,huperzine A（10-6 and 10-5mol·L-1） also decreased MGO induced caspase 3 activity increasing.CONCLUSION Huperzine A protected MGO induced injury in the cultured HBMEC,which may be involved its anti-oxidation and anti-apoptosis activity.