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目的:探讨罗格列酮对人胃癌MGC803细胞凋亡的影响及其分子机制。方法:吖啶橙(AO)荧光染色和流式细胞仪分析检测细胞凋亡。同时行bax和bcl-2细胞免疫化学染色和定量分析。结果:罗格列酮能诱导MGC803细胞凋亡,且随着浓度增加,其凋亡率逐渐增加。罗格列酮(25μmol/L、50μmol/L)作用于人胃癌MGC803细胞48h后bax表达的光密度值由0·10±0·02分别升至0·42±0·03、0·75±0·04,P=0·000;bcl-2表达的光密度值由0·51±0·02分别降至0·25±0·04、0·12±0·01,P=0·001。结论:罗格列酮能诱导人胃癌MGC803凋亡,其机制可能与bax基因表达上调、bcl-2基因表达下调有关。
Objective: To investigate the effect of rosiglitazone on the apoptosis of human gastric cancer cell line MGC803 and its molecular mechanism. Methods: Apoptosis was detected by acridine orange (AO) staining and flow cytometry. Immunohistochemical staining and quantitative analysis of bax and bcl-2 cells simultaneously. Results: Rosiglitazone induced apoptosis in MGC803 cells, and the apoptosis rate increased with the increase of concentration. After treated with rosiglitazone (25μmol / L, 50μmol / L) for 48h, the optical density of bax increased from 0 · 10 ± 0 · 02 to 0 · 42 ± 0 · 03,0 · 75 ± 0 · 04, P = 0.000; the optical density of bcl-2 expression decreased from 0 · 51 ± 0 · 02 to 0 · 25 ± 0 · 04 and 0 · 12 ± 0 · 01, P = 0 · 001 . CONCLUSION: Rosiglitazone can induce apoptosis of human gastric cancer MGC803, which may be related to upregulation of bax gene expression and down-regulation of bcl-2 gene expression.