Xia Dan
Nat Prod Commun. 2015 Feb;10(2):249-52.
The effect and mechanism of ovarian cancer HO-8910 cell apoptosis induced by crocin.MTT assay was performed to detect the inhibitory action of crocin on the proliferation of HO-8910 cells. Flow cytometry was used to test the cell cycle distribution and apoptosis rate of ovarian cancer HO-8910 cells. Western blot analysis was utilized to measure the levels of apoptotic proteins such as p53, Fas/APO-1, and Caspase-3. MTT analysis revealed that crocin significantly inhibited the growth of HO-8910 cells. Additionally, flow cytometry illustrated that crocin raised the proportion of HO-8910 cells in the G0/G1 phase and increased their apoptosis rate. Furthermore, Western blot analysis revealed that crocin up-regulated the expression of p53, Fas/APO-1, and Caspase-3. The results of this study showed that crocin can significantly inhibit the growth of HO-8910 cells and arrest them in the G0/G1 phase. Crocin can also promote ovarian cancer HO-8910 cell apoptosis, most likely by increasing p53 and Fas/APO-1 expression, and then activating the apoptotic pathway regulated by Caspase-3.
西红花苷诱导卵巢癌HO-8910细胞凋亡的作用及机制。采用MTT法检测西红花苷对HO-8910细胞增殖的抑制作用。运用流式细胞术检测卵巢癌HO-8910细胞的细胞周期分布及凋亡率。利用蛋白质免疫印迹分析检测p53、Fas/APO-1和Caspase-3等凋亡蛋白的水平。MTT分析显示,西红花苷显著抑制HO-8910细胞的生长。此外,流式细胞术表明,西红花苷提高了HO-8910细胞在G0/G1期的比例并增加了其凋亡率。再者,蛋白质免疫印迹分析显示,西红花苷上调了p53、Fas/APO-1和Caspase-3的表达。本研究结果表明,西红花苷可显著抑制HO-8910细胞的生长并使其停滞于G0/G1期。西红花苷还可促进卵巢癌HO-8910细胞凋亡,很可能是通过增加p53和Fas/APO-1的表达,进而激活由Caspase-3调控的凋亡途径。