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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 study the protective effect and mechanism of huperzine A on human brain microvascular endothelial cells (HBMEC) in vitro. Methods Cultured HBMEC cells were induced with pyruvate, and cell viability was measured by MTT assay. LDH, SOD activity kit and caspase-3 activity kit were used to detect cell injury, and the mechanism and action of huperzine A were observed. Results Huperzine A could protect MGO-induced cell injury in a concentration-dependent manner, with maximum protective effect at 10-5 mol·L-1. Acetone aldehyde could induce the decrease of SOD activity of HBMEC, but Huperzine A (10-6,10-5 mol·L-1) could reverse this effect. Further study found huperzine A can inhibit pyruvate-induced caspase-3 activity. Conclusion Huperzine A has a protective effect on pyruvate-induced HBMEC injury, which may be related to its anti-free radical and anti-apoptotic effects.