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目的:探讨Rg3抑制人腺样囊性癌细胞的作用及其诱导凋亡的机制。方法:用一定质量浓度的Rg3处理人腺样囊性癌细胞系SACC-83细胞,MTT法检测细胞增殖活力,荧光显微镜下观察凋亡细胞的形态,流式细胞仪分析细胞周期和细胞增殖指数,免疫组织化学观察hTERT的表达变化。结果:Rg3抑制SACC-83细胞生长,呈时间-浓度效应关系;经20 mg.L-1 Rg3处理细胞24,48 h后,观察到典型的凋亡细胞形态,即染色质凝集、核片段化、凋亡小体、核内致密的颗粒状荧光;用不同浓度的Rg3处理细胞72 h后,均诱导了细胞凋亡和细胞周期的改变,G0/G1的细胞比率增加,S期和G2/M期的细胞比率下降,细胞增殖指数降低,并与Rg3浓度有明显依赖关系;免疫组化染色显示Rg3抑制了SACC-83细胞的hTERT蛋白表达。结论:Rg3可通过诱导人腺样囊性癌细胞SACC-83细胞凋亡和下调细胞的端粒酶活性,使细胞增殖受到抑制。
Objective: To investigate the role of Rg3 in inhibiting human adenoid cystic carcinoma cells and the mechanism of its induction of apoptosis. METHODS: Human adenoid cystic carcinoma cell line SACC-83 cells were treated with Rg3 at a certain concentration. Cell viability was measured by MTT assay. Morphology of apoptotic cells was observed under fluorescence microscope. Cell cycle and cell proliferation index were analyzed by flow cytometry. The expression of hTERT was observed by immunohistochemistry. RESULTS: Rg3 inhibited the growth of SACC-83 cells in a time-concentration-dependent manner. After treatment with 20 mg.L-1 Rg3 for 24 and 48 h, typical apoptotic cell morphology was observed, ie chromatin condensation and nuclear fragmentation. Apoptotic bodies, dense granular fluorescence in the nucleus; cells treated with different concentrations of Rg3 for 72 h all induced apoptosis and cell cycle changes, and the cell ratio of G0/G1 increased, S phase and G2/ The cell ratio in M phase decreased, the cell proliferation index decreased, and it had a significant dependence on Rg3 concentration. Immunohistochemical staining showed that Rg3 inhibited the hTERT protein expression in SACC-83 cells. CONCLUSION: Rg3 can inhibit the proliferation of human adenoid cystic carcinoma cells SACC-83 cells and down-regulate the telomerase activity of cells.