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目的观察苦瓜蛋白诱导K562细胞凋亡时细胞粘附分子(CD54、CD44)表达水平的变化,探讨粘附分子在苦瓜蛋白诱导K562细胞凋亡中的作用。方法以一定浓度的苦瓜蛋白处理K562细胞;CCK-8试剂盒检测其对细胞生长的影响;流式细细术(An-nexinⅤ)、透射电镜等方法检测细胞凋亡;同时应用流式细细术检测粘附分子(CD54、CD44)蛋白表达水平的变化。结果苦瓜蛋白对K562细胞生长具有明显的抑制作用;流式细胞术及形态学观察(电镜)证实一定作用浓度的苦瓜蛋白可诱导K562细胞发生明显的细胞凋亡;苦瓜蛋白处理组K562细胞中CD54、CD44表达分别为18.62%和1.32%,对照组分别为0.25%和0.17%,分别上调了18.37%、1.15%。结论苦瓜蛋白引起K562细胞凋亡的过程中,粘附分子CD54表达上调;CD54表达上调可能是苦瓜蛋白诱导肿瘤细胞凋亡的机制之一,其机制可能涉及细胞粘附依赖性细胞凋亡。
Objective To observe the changes of cell adhesion molecules (CD54, CD44) in the apoptosis of K562 cells induced by bitter melon and to explore the role of adhesion molecules in the apoptosis of K562 cells induced by bitter melon. Methods K562 cells were treated with a certain concentration of bitter melon protein. The effects of CCK-8 on cell growth were detected by flow cytometry (A-nexin V) and transmission electron microscopy. Flow cytometry The changes of protein expression of adhesion molecules (CD54, CD44) were detected. Results Momordica charantia inhibited the growth of K562 cells. Flow cytometry and morphological observation (electron microscopy) showed that certain concentrations of Momordin could induce apoptosis in K562 cells. CD54 , Respectively. The expression of CD44 was 18.62% and 1.32% respectively, while the control group was 0.25% and 0.17% respectively, up-regulated by 18.37% and 1.15% respectively. CONCLUSION: MAPK up-regulates the expression of adhesion molecule CD54 during the apoptosis of K562 cells induced by bitter gourd protein. The up-regulation of CD54 expression may be one of the mechanisms of apoptosis induced by bitter gourd protein. The possible mechanism may be cell adhesion-dependent apoptosis.