6-Shogaol Induces Autophagy and Apoptosis in Human colon adenocarcinoma HT-29 Cells

• Main Authors: Ting-Yi Li, 李亭逸
• Other Authors: Been-Huang Chiang
• Format: Others
• Language: zh-TW
• Published: 2012
• Online Access: http://ndltd.ncl.edu.tw/handle/90595806043324472515

碩士 === 國立臺灣大學 === 食品科技研究所 === 100 === 　Autophagic cell death (Type II programmed cell death) and apoptosis (Type I programmed cell death) are two distinct forms of cell death. They have a complex functional relationship in the sense that, autophagy constitutes a stress adaptation that avoids cell death (and suppresses apoptosis) and an alternative cell-death pathway. Ginger, have several phenolic alkanones among which 6-shogaol is shown to exert anti-inflammatory, anti-bacterial and anti-hepatotoxic properties. Also it has been shown to induce apoptosis in human colorectal carcinoma cells. In our previous studies, we found that 6-shogaol can induce apoptosis of HT-29 (human colorectal carcinoma cells) via modulation of mitochondrial functions. In this study, we assumed that the cell growth inhibition activity of 6-shogaol on the HT-29 is via both autophagy and apoptosis. The results showed that in the survival test, within 24 hrs treatment, effect of 6-shogaol on cell survival rate was not dose dependent. Then we used flow cytometry to analyze the autophagososome and auto- lysosome activity and did a series of apoptosis test, including Annexin-V, caspase3 / 7 activation, DNA fragment. Also, the confocal microscopy showed the formation of autophagososome which proved that the occurrence of autophagy and apoptosis was originally determined by the different doses and time points. That is, both cell death types go hand in hand and can be divided at 18 h. Autophagy can be maintained a bit longer in the low concentration (20 μM), but at high concentration (80 μM), both of autophagic death and apoptosis play significant roles. In addition, 6-shogaol which induces the G2 / M cell cycle arrest, it can be speculated that 6-shogaol affect cell mitosis and promote cell death.