CAJ | 학술논문

目的：研究骨碎补总黄酮对MLO-Y4类骨细胞系增殖、分化、矿化以及凋亡的影响。方法体外培养MLO-Y4细胞，并以MC3T3-E1细胞作对照细胞，分别用不同质量浓度（1，10，100 mg／l）的骨碎补总黄酮干预，采用CCK-8法以及ALP试剂盒检测MLO-Y4细胞的增殖和分化情况；用茜素红染色法观察矿化结节的形成；DAPI染色和流式细胞术定性和定量反映依托泊苷诱导的细胞凋亡情况。结果1，10 mg／l浓度组的骨碎补总黄酮能促进MLO-Y4细胞的增殖，并且能够一定程度上促进细胞ALP的合成分泌，100 mg／l组不具有促进细胞增殖，ALP合成分泌的作用。三个浓度组均无影响MLO-Y4细胞钙结节形成的作用。1，10 mg／l组对依托泊苷诱导的细胞凋亡具有一定的抑制作用，100 mg／l组则相反。结论一定浓度的骨碎补总黄酮对MLO-Y4细胞的增殖，分化有一定的促进作用，并能够抑制其凋亡。
목적：연구골쇄보총황동대MLO-Y4류골세포계증식、분화、광화이급조망적영향。방법체외배양MLO-Y4세포，병이MC3T3-E1세포작대조세포，분별용불동질량농도（1，10，100 mg／l）적골쇄보총황동간예，채용CCK-8법이급ALP시제합검측MLO-Y4세포적증식화분화정황；용천소홍염색법관찰광화결절적형성；DAPI염색화류식세포술정성화정량반영의탁박감유도적세포조망정황。결과1，10 mg／l농도조적골쇄보총황동능촉진MLO-Y4세포적증식，병차능구일정정도상촉진세포ALP적합성분비，100 mg／l조불구유촉진세포증식，ALP합성분비적작용。삼개농도조균무영향MLO-Y4세포개결절형성적작용。1，10 mg／l조대의탁박감유도적세포조망구유일정적억제작용，100 mg／l조칙상반。결론일정농도적골쇄보총황동대MLO-Y4세포적증식，분화유일정적촉진작용，병능구억제기조망。
Objective To investigate the effect of drynaria total flavonoids on the proliferation, differentiation, mineralization, and apoptosis of MLO-Y4 cells.Methods MLO-Y4 cells were cultured with different concentrations (1, 10, 100 mg/l) of drynaria total flavonoids in vitro, and MC3T3-E1 cells were cultured as a control.The proliferation and differentiation of MLO-Y4 cells were examined using CCK-8 method and the alkaline phosphatase ( ALP) kit, respectively.The mineralization was detected using Alizarin red staining.DAPI staining and flow cytometry were used to reflect the cell apoptosis induced by etoposide.Results The most effective concentration of the drynaria total flavonoids on the proliferation and differentiation of MLO-Y4 cells were 1 mg/l and 10 mg/l, respectively.The concentration of 100mg/l did not stimulate cell proliferation and ALP activity.There was no effect on the formation of calcium nodules with all concentrations.Concentrations of 1 and 10 mg/l inhibited the apoptosis to a certain extent.In contrary, concentration of 100 mg/l played a role in invoking cell apoptosis.Conclusion Certain concentrations of drynaria total flavonoids can promote the proliferation and differentiation of MLO-Y4 cells, and can inhibit the cell apoptosis.