Anticancer effect by the combination of grape seed extract or ellagic acid with chemotherapeutic agents in colorectal carcinoma

• Main Authors: Yin-Wen Tsai, 蔡姎紋
• Other Authors: Ting-Yu Kao
• Format: Others
• Language: zh-TW
• Online Access: http://ndltd.ncl.edu.tw/handle/pp38gj

碩士 === 元培科技大學 === 醫學檢驗生物技術研究所 === 100 === Ellagic acid (EA) inhibits the proliferation and apoptosis on the treated cancer cell, which is rich in natural fruits, such as pomegranates, phyllanthus urinaria, and longan, etc. In recent years, animal experiment has confirmed the anti-oxide ability of ellagic acid on the decrease in many side effects led by Cisplatin. Grape seed extract(GSE) is one of the most nutritional supplements taking by cancer patients in last two decade. Research in nearly a decade has confirmed that it is rich in procyanidins, and inhibits the proliferation and apoptosis on the treated cancer cell. Animal experiment has also confirmed the anti-oxide ability to decrease many side effects led by chemotherapy drug. However, there is no report revealed the synergy effect of the colorectal carcinoma chemotherapy drugs while combining with GSE or EA, neither the molecular mechanism. In this thesis, the different-stage cell lines of colorectal carcinoma as a model, including the SW480 and HT-29 in second stage and the LoVo and Colo 320DM in third stage, are treated with colorectal carcinoma chemotherapy drugs (5-Fluorouracil,Oxaliplatin or Irinotecan) combing separately with GSE or EA. The analyses are based on trypan blue stain for cell viability, Rhodamine 123 for mitochondrial membrane potential, Annexin V labeling for apoptosis, and immunoblotting for change in the levels of proteins involved in cell apoptosis. The experiment result shows as follows: The combinations of the the chemotherapy drugs with GSE or EA, exist inhibition on cell proliferation by cell viability. There is no obvious change for combination with GSE, while significantly increase for that with EA on mitochondrial membrane potential. The comparison between the control group and HT-29 treated with both EA (83 μM) and 5-Fluorouracil expresses significantly increased for Bax and cleaved PARP, and decreased for Bcl-2, procaspase-3 and PARP. For LoVo cells treated with EA (83μM) and Oxaliplatin, Bax and Bcl-2 have no significant change, while procaspase-3 and PARP decreased, and the cleaved PARP increased. For Colo 320DM cells treated with EA (83μM) and Irinotecan, Bcl-2 has no change, procaspase-3 and PARP decreased, while both Bax and the cleaved RARP increased. Conclusion suggests that: The combination group of GSE inhibits on cell survival, but the mechanism requires further confirm. The inhibiting of cell proliferation and the inducing of cell apoptosis through both the chemotherapy drug and EA have been confirmed, that has the potential for treatment on colorectal carcinoma in the future.