領學術科研之先,創(chuàng)食品科技之新
—— 中國食品雜志社
期刊集群
Influence of luteolin on the apoptosis of esophageal cancer Eca109 cells and its mechanism of action
來源:食品科學網(wǎng) 閱讀量: 379 發(fā)表時間: 2019-09-25
作者: Shaokang Wang, Lingmeng Fu, YiWu, Hongmei Xiao, Jing Wang, Guiju Sun?
關鍵詞: Esophageal cancer,Luteolin,Apoptosis
摘要:

The present study was conducted to verify the influence of luteolin on apoptosis of Eca109 cells and to

further investigate the possible mechanisms underlying its effect on apoptosis. The cells were exposed

to different concentrations of luteolin (0, 40, 80, 120, 160, 200, 240 M) for 24, 48, and 72 h respectively.

The influence of luteolin on proliferation of Eca109 cells was detected using MTT assay. Eca109 cells were

then treated with luteolin (0, 40, 160, 240 M) for 24 h. The effect of luteolin on cell cycle progression

and apoptosis was assayed by using flow cytometry (FCM). Expression of caspase9 and caspase3 mRNA

and protein was analyzed by real-time PCR and Western blot respectively. The results showed that luteolin

could inhibit the proliferation of Eca109 cells at all concentrations in a time-dependent manner and

the relative inhibition rate showed an inverted U-shaped association with the concentration of luteolin.

Further, the cell cycle was arrested in the S phase following treatment with luteolin. Apoptosis analysis

indicated that luteolin could induce the apoptosis of Eca109 cells across the three concentration

groups, which exhibited a trend of first promotional and then inhibitory with the increases in luteolin

concentration. The effect of luteolin on the mRNA and protein expression of caspase 9 and caspase3 first

manifested as promotion, then inhibition. Therefore, luteolin may serve a role in promoting cell apoptosis

by inducing Eca109 cell apoptosis that involves the expression of caspase3, caspase9 mRNA and protein.

This study provides theoretical basis for further study and clinical application of luteolin. The specific

mechanism has not yet been clarified and the other activation pathways inducing apoptosis need to be

further studied.

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