期刊論文
學年 | 93 |
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學期 | 1 |
出版(發表)日期 | 2004-09-01 |
作品名稱 | Comparison of radical scavenging activity, cytotoxic effects and apoptosis induction in human melanoma cells by Taiwanese propolis from different sources |
作品名稱(其他語言) | |
著者 | 吳嘉麗; Wu, Chia-li; Chen, Chia-nan; Weng, Meng-shih; Lin, Jen-kun |
單位 | 淡江大學化學學系 |
出版者 | New York: Oxford University Press |
著錄名稱、卷期、頁數 | Evidenced-based Complementary and Alternative Medicine 1(2), pp.175-185 |
摘要 | Propolis is a sticky substance that is collected from plants by honeybees. We previously demonstrated that propolins A, B, C, D, E and F, isolated from Taiwanese propolis (TP), could effectively induce human melanoma cell apoptosis and were strong antioxidant agents. In this study, we evaluated TP for free radical scavenging activity by DPPH (1,2-diphenyl-2-picrylhydrazyl). The phenolic concentrations were quantified by the Folin–Ciocalteu method. The apoptosis trigger activity in human melanoma cells was evaluated. TP contained a higher level of phenolic compounds and showed strong capability to scavenge free radicals. Additionally, TP1g, TP3, TP4 and TP7 exhibited a cytotoxic effect on human melanoma cells, with an IC50 of ∼2.3, 2.0, 3.3 and 3.3 μg/ml, respectively. Flow cytometric analysis for DNA fragmentation indicated that TP1g, TP2, TP3 and TP7 could induce apoptosis in human melanoma cells and there is a marked loss of cells from the G2/M phase of the cell cycle. To address the mechanism of the apoptosis effect of TP, we evaluated its effects on induction of apoptosis-related proteins in human melanoma cells. The levels of procaspase-3 and PARP [poly(ADP-ribose) polymerase] were markedly decreased. Furthermore, propolins A, B, C, D, E and F in TP were determined using HPLC. The results indicate that TP is a rich source of these compounds. The findings suggest that TP induces apoptosis in human melanoma cells due to its high level of propolins. |
關鍵字 | |
語言 | en |
ISSN | 1741-427X |
期刊性質 | 國外 |
收錄於 | |
產學合作 | |
通訊作者 | |
審稿制度 | |
國別 | USA |
公開徵稿 | |
出版型式 | 紙本 |
相關連結 |
機構典藏連結 ( http://tkuir.lib.tku.edu.tw:8080/dspace/handle/987654321/24883 ) |