二氢杨梅素诱导人卵巢癌HO-8910细胞凋亡及机制研究

目的二氢杨梅素体外对人卵巢癌HO-8910细胞生长、凋亡的影响，及其作用机制的探讨。方法体外培养HO-8910细胞，以不同浓度(10、20、40 μmol/L)的二氢杨梅素作用于HO-8910细胞，MTT法及CCK-8法检测对细胞生长的抑制作用；AnnexinV-FITC/PI双染流式细胞仪检测对细胞凋亡的影响；Hoechst 33258荧光染色观察细胞凋亡情况；Western blotting法检测Caspase-3、Bcl-2、Bax、ERK、p-ERK蛋白表达情况。结果MTT和CCK-8结果均显示二氢杨梅素可浓度依赖性地抑制HO-8910细胞的生长；流式细胞仪结果显示二氢杨梅素可浓度依赖性促进HO-8910细胞凋亡；Hoechst 33258荧光染色结果显示，二氢杨梅素作用后的HO-8910细胞呈现典型凋亡形态学改变；Western blotting结果显示二氢杨梅素可上调HO-8910细胞Caspase-3和Bax水平，下调Bcl-2、ERK、p-ERK水平(P < 0.05)。结论二氢杨梅素具有抗人卵巢癌HO-8910细胞活性的作用，并诱导其凋亡，其作用机制与调控ERK/MAPK信号通路有关。

Study on the apoptosis induced by dihydromyricetin in human ovarian cancer HO-8910 cells and its mechanism

ObjectiveTo investigate the effects of dihydromyricetin on the growth and apoptosis of human ovarian cancer HO-8910 cells, and its mechanism.MethodsThe HO-8910 cells were cultured in vitro, and treated with dihydromyricetin at different concentrations(10, 20 and 40 μmol/L).The proliferation of cells was detected using MTT and CCK-8 method, the apoptosis of cells was detected using the Annexin V-FITC/PI flow cytometry and Hoechst 33258 fluorescence staining, and the expression levels of Caspase-3, Bcl-2, Bax, ERK and p-ERK protein were detected using Western blotting.ResultsThe results of MTT and CCK-8 was showed that dihydromyricetin could inhibit the growth of HO-8910 cells in a concentration-dependent manner.The results of flow cytometry showed that dihydromyricetin could promote the HO-8910 cell apoptosis in a concentration-dependent manner.The typical morphological changes of apoptosis in HO-8910 cells treated with dihydromyrmectin were found using Hoechst 33258 fluorescence staining.The results of Western blotting showed that dihydromyricetin could up-regulate the levels of Caspase-3 and Bax, and down-regulate the levels of Bcl-2, ERK and p-ERK in HO-8910 cells(P < 0.05).ConclusionsDihydromyricetin can inhibit the activity of human ovarian cancer HO-8910 cells and induce their apoptosis, and the mechanism of which is related to the regulation of ERK/MAPK signaling pathway.