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目的 研究牛脑微血管内皮细胞(BCMEC)过氧化损伤机制并探讨羟乙基葛根素对牛脑微血管内皮细胞 损伤的保护作用。方法用MTT法和LDH活性检测测定BCMEC的损伤;倒置相差显微镜下一般形态学观察、透射电子显微镜超微结构观察及流式细胞术测定BCMEC凋亡变化。结果 H2O2(200μmol·L-1)损伤BCMEC后,细胞存活率下降,LDH释放增加,羟乙基葛根素和edaravone可减轻此损伤。H2O2(100μmol·L-1)可诱导BCMEC凋亡, 羟乙基葛根素和edaravone对此有保护作用。结论羟乙基葛根素和edaravone对H2O2导致的BCMEC坏死和凋亡 有保护作用,该作用与其抗氧化作用有关。
Objective To study the mechanism of peroxidative injury of bovine brain microvascular endothelial cells (BCMEC) and explore the protective effect of hydroxyethylpuerarin on the damage of bovine brain microvascular endothelial cells. Methods MTT assay and LDH activity assay were used to determine the damage of BCMEC. General morphological observation under inverted phase contrast microscope, ultrastructure observation by transmission electron microscopy and flow cytometry were used to determine the apoptosis of BCMEC. Results After H2O2(200μmol·L-1) damage BCMEC, cell survival rate decreased, LDH release increased, hydroxyethylpuerarin and edaravone can reduce this injury. H2O2 (100 μmol·L-1) can induce apoptosis of BCMEC, and hydroxyethylpuerarin and edaravone have protective effects. Conclusion Hydroxyethylpuerarin and edaravone have protective effects on H2O2-induced necrosis and apoptosis of BCMEC, and this effect is related to its antioxidation.