藏红花水提取物抑制人卵巢癌细胞HO-8910的增殖作用

本文研究了藏红花水提取物抑制HO-8910人卵巢癌细胞的增殖作用。将实验分为细胞组、藏红花水提物低剂量组（0.4 mg/L）、中剂量组（0.8 mg/L）、高剂量组（1.0 mg/L），HO-8910细胞培养成功后，分别用不同浓度的藏红花水提物进行处理，检测卵巢癌细胞的增殖能力及细胞外调节蛋白激酶（ERK）、Bcl-2、Bax蛋白的含量。结果表明，在实验浓度范围内，随着藏红花水提物浓度的提高，卵巢癌细胞的增长率明显受到抑制，其中，高剂量组作用时，24 h、48 h、72 h的增殖率分别为14.13%、12.15%、和11.16%，显著低于其他各实验组（p<0.05）；另外，高剂量组藏红花水提物作用后，其对卵巢癌细胞的凋亡率以及对癌细胞侵袭能力的抑制率分别为20.11%和64.24%，其ERK、Bcl-2、Bax蛋白表达量分别为0.61、0.48和0.95，与其他实验组均具有显著性差异（p<0.05）。说明藏红花水提取物能够明显抑制卵巢癌细胞活性，降低卵巢癌细胞增殖能力及侵袭能力，其作用机制可能与ERK信号通路有关。

Inhibitory Effect of Saffron Water Extract on Proliferation of Human Ovarian Cancer Cell Line HO-8910

The inhibitory effect of saffron water extract on the proliferation of HO-8910 human ovarian cancer cell was investigated. The experiment was divided into cell group, saffron water extract low-dose group (0.4 mg/L), medium dose group (0.8 mg/L) and high-dose group (1.0 mg/L). After HO-8910 cells were successfully cultured, they were treated with different concentrations of affron water extract. The proliferation ability of ovarian cancer cells and the content of extracellular regulated protein kinase (ERK), Bcl-2 and Bax protein were detected. The results showed that in the experimental concentration range, the growth rate of ovarian cancer cells was significantly inhibited with the increase of saffron water extract concentration. At 24 h, 48 h and 72 h, the proliferation rates of high dose group were 14.13%, 12.15%, and 11.16%, respectively, which were significantly lower than those of other experimental groups (p<0.05). Furthermore, the inhibition rates of saffron water extract on ovarian cancer cell apoptosis and invasion were 20.11% and 64.24%, respectively. The protein expression levels of ERK, Bcl-2 and Bax were 0.61, 0.48 and 0.95, respectively, which were significantly different than those of other experimental groups (p<0.05). These results indicated that saffron water extract could significantly inhibit the activity of ovarian cancer cells, reduce the proliferation and invasion ability of ovarian cancer cells, and its mechanism might be related to ERK signaling pathway.