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目的为研究野西瓜极性生物碱(Capparis spinosa L.polar alkaloid)诱导人肝癌细胞HepG-2细胞凋亡的线粒体机制,观察了野西瓜极性生物碱对HepG-2细胞内活性氧(reactive oxygen species,ROS)、Ca2+浓度和Caspase-9,3的影响。方法经流式细胞仪观察野西瓜极性生物碱对活性的影响;激光共聚焦显微镜检测野西瓜极性生物碱作用前后,HepG-2细胞内Ca2+浓度的变化;酶标仪检测Caspase-9,3活性。结果野西瓜极性生物碱可不同程度的升高HepG-2细胞活性氧水平和Ca2+浓度,还可以引起Caspase-9,3活性的增加。结论野西瓜极性生物碱引起HepG-2细胞内活性氧增加,造成细胞内Ca2+超载,启动Caspase级联反应,诱导HepG-2细胞凋亡。
Aim To investigate the mitochondrial mechanism of apoptosis in HepG-2 cells induced by Capparis spinosa L.polar alkaloid and observe the effect of polar alkaloids from Radix et Rhizoma meloni on reactive oxygen species in HepG-2 cells species, ROS), Ca2 + concentration and Caspase-9,3. Methods The effect of polar alkaloids of wild watermelon on the activity was observed by flow cytometry. The changes of Ca2 + concentration in HepG-2 cells before and after the action of polar alkaloids were detected by laser scanning confocal microscopy. The expressions of Caspase-9, 3 activity. Results Wild Alkaloid alkaloids could increase the levels of reactive oxygen species and Ca2 + in HepG-2 cells to varying degrees and also increase the activity of Caspase-9,3. Conclusion The alkaloids from wild watermelon induced the increase of reactive oxygen species (ROS) in HepG-2 cells, resulting in overloading of intracellular Ca2 +, activation of caspase cascade and induction of apoptosis in HepG-2 cells.