二氢杨梅素通过ERK和p38途径抑制人胃癌AGS细胞的增殖并诱导其凋亡

Inhibition of Cell Proliferation by Dihydromyricetin Through ERK and p38 Pathways in Human Gastric Cancer AGS Cells

目的研究二氢杨梅素对人胃癌AGS细胞增殖的抑制功效及其机制。方法取对数生长期的胃癌AGS细胞,分别用10、20、40和80μmol/L的二氢杨梅素共培养处理,采用MTT实验检测细胞活力,磷脂结合蛋白V/PI染色和活性胱天蛋白酶测定细胞凋亡程序,Western-blot检测凋亡相关蛋白的表达。结果当二氢杨梅素浓度为10~80μmol/L时,胃癌AGS细胞的增殖受到剂量依赖性抑制;经二氢杨梅素处理后,AGS细胞的总凋亡数量与样品浓度呈剂量依赖性;当二氢杨梅素浓度为80μmol/L时,胃癌AGS细胞的p-ERK/ERK蛋白的水平降低了81.5%,而p-p38/p38蛋白的水平降低了78.6%。结论二氢杨梅素可显著抑制胃癌细胞AGS的增殖,其机制可能是通过调控丝裂原活化蛋白激酶的家族成员ERK和p38的表达,抑制人胃癌AGS细胞的增殖并诱导其凋亡。

Objective To study the anti-proliferative effect and mechanism of dihydromyricetin on human gastric cancer AGS cells.Method We took logarithmic growth phase gastric cancer AGS cells and treat them with 10,20,40,and 80μmol/L of dihydromyricetin.MTT assay was used to test cell viability.Phospholipid-binding protein V/PI staining and active caspase kit assay were used to test the cell apoptosis process.and Western blot was used to analyze the protein expressions related to cell apoptosis.Results When the concentration of dihydromyricetin was 10-80μmol/L,the proliferation of gastric cancer AGS cells was inhibited in a dose-dependent manner while the total number of apoptosis of AGS cells was presented as the same trends.On the other hand,the level of p-ERK/ERK protein in AGS cells decreased by 81.5%.And expression of p-p38 protein decreased by 78.6%compared with the control.Conclusion The addition of dihydromyricetin can significantly inhibit the proliferation of gastric cancer AGS cells through the modulation of mitogen activated protein kinase family,ERK and p38,to inhibit the proliferation of human gastric cancer AGS cells and induce their apoptosis.