World Journal of Gastroenterology, 2004, 10(12):1822-1825.

Apoptosis of human primary gastric carcinoma cells induced by genistein

Hai-Bo Zhou, Juan-Juan Chen, et al

Department of Gastroenterology, Second Affiliated Hospital of Zhejiang University, Hangzhou 310009, Zhejiang Province, China

AIM: To investigate the apoptosis in primary gastric cancer cells induced by genistein, and the relationship between this apoptosis and expression of bcl-2 and bax.

METHODS: MTT assay was used to determine the cell growth inhibitory rate in vitro. Transmission electron microscope and TUNEL staining were used to quantitatively and qualitatively detect the apoptosis of primary gastric cancer cells before and after genistein treatment. Immunohistochemical staining and RT-PCR were used to detect the expression of apoptosis-associated genes bcl-2 and bax.

RESULTS: Genistein inhibited the growth of primary gastric cancer cells in dose-and time-dependent manner. Genistein induced primary gastric cancer cells to undergo apoptosis with typically apoptotic characteristics. TUNEL assay showed that after the treatment of primary gastric cancer cells with genistein for 24 to 96 h, the apoptotic rates of primary gastric cancer cells increased time-dependently. Immunohistochemical staining showed that after the treatment of primary gastric cancer cells with genistein for 24 to 96 h, the positivity rates of Bcl-2 proteins were apparently reduced with time and the positivity rates of Bax proteins were apparently increased with time. After exposed to genistein at 20 μmol/L for 24, 48, 72 and 96 respectively, the density of bcl-2 mRNA decreased progressively and the density of bax mRNA increased progressively with elongation of time.

CONCLUSION: Genistein is able to induce the apoptosis in primary gastric cancer cells. This apoptosis may be mediated by down-regulating the apoptosis- associated bcl-2 gene and up-regulating the expression of apoptosis-associated bax gene.

中国《世界胃肠病杂志》，2004年

金雀异黄素诱导人原发性胃癌细胞凋亡

周海波，陈娟娟，等

浙江大学第二附属医院消化内科，浙江杭州

目的：调查染料木黄酮诱导的原发性胃癌细胞凋亡及其与bcl-2和bax表达的关系。

方法：MTT法检测体外细胞生长抑制率。使用透射电子显微镜和TUNEL染色来定性和定性检测染料木素治疗前后原发性胃癌细胞凋亡。免疫组织化学染色和RT-PCR检测凋亡相关基因bcl-2和bax的表达。

结果：染料木黄酮以剂量和时间依赖的方式抑制原发性胃癌细胞的生长。染料木黄酮诱导原发性胃癌细胞经历凋亡，具有典型的凋亡特征。 TUNEL检测显示，用染料木素治疗原发性胃癌细胞24〜96 h后，原发性胃癌细胞的凋亡率随时间而变化。免疫组织化学染色显示，用染料木素治疗原发性胃癌细胞24〜96 h后，Bcl-2蛋白的阳性率明显降低，Bax蛋白阳性率随时间明显增加。分别暴露于20μmol/ L的染料木素后，bcl-2 mRNA的密度逐渐降低，bax mRNA的密度随着时间的延长逐渐增加。

结论：染料木黄酮能够诱导原发性胃癌细胞凋亡。这种细胞凋亡可能通过下调细胞凋亡相关bcl-2基因和上调凋亡相关bax基因的表达来介导。