玉檀木超臨界萃取物對人類肺腺癌細胞生長、移行與侵襲之抑制效果 = Inh...
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  • 玉檀木超臨界萃取物對人類肺腺癌細胞生長、移行與侵襲之抑制效果 = Inhibitory effects of Bulnesia sarmientoi supercritical fluid extract on the proliferation, migration and invasion of human lung adenocarcinoma cells
  • 紀錄類型: 書目-語言資料,印刷品 : 單行本
    並列題名: Inhibitory effects of Bulnesia sarmientoi supercritical fluid extract on the proliferation, migration and invasion of human lung adenocarcinoma cells
    作者: 張榮哲,
    其他團體作者: 國立高雄大學
    出版地: [高雄市]
    出版者: 撰者;
    出版年: 2014[民103]
    面頁冊數: 121面圖,表 : 30公分;
    標題: 玉檀木
    標題: Bulnesia sarmientoi
    電子資源: http://handle.ncl.edu.tw/11296/ndltd/62099856308695924194
    附註: 106年4月25日公開
    附註: 參考書目:面95-112
    摘要註: 玉檀木是一種成長緩慢的硬木樹種,主要分佈於南美洲,其傳統療效為消風、熱、毒之功用,以及促使皮膚癒合、開胃、利脾、作為大腦興奮劑等,且有研究指出玉檀木具有抗發炎及抗癌等生理活性。本研究目的是利用體外細胞培養模式,研究以超臨界萃取之玉檀木萃取物 (BSE) 對人類肺腺癌細胞A549、H661、H1299 與人類正常胚胎肺纖維細胞 MRC-5的生長抑制作用及誘導細胞壞死之效應。實驗結果顯示,在處理時間為48 hr 之條件下, BSE 對A549、H661和 H1299 細胞之毒殺IC50 值分別為 43.7、44.6 和53.3 μg/ml,且隨劑量增加,其抑制癌細胞生長的作用愈明顯;相對地,BSE 對 MRC-5 正常細胞的毒殺作用則較低,其 IC50 值為 89.7 μg/ml。再者,BSE 處理時間與癌細胞生長的抑制程度呈正相關,顯示其為一長效型抑癌劑。在細胞週期與細胞凋亡分析方面,BSE 會促使肺癌細胞停滯於 G2/M 生長期。進一步利用Annexin-V-FITC/PI 進行細胞凋亡分析,實驗結果顯示BSE 主要誘導細胞走向壞死。經西方墨點法進一步確認,BSE 會向上調節TNF-α、RIP-1與RIP-3 等促程序性壞死蛋白的表現,並向下調節抗程序性壞死蛋白caspase-8 的表現,證實BSE 會誘導肺癌細胞走向程序性細胞壞死的路徑。此外,由細胞遷移、移行與侵襲試驗結果顯示,BSE有抑制 A549、H661 細胞轉移之能力,並由西方墨點法進一步確認BSE 的處理會抑制MMP-2 及MMP-9 促轉移蛋白的表現。綜合本研究的結果,由於BSE對 A549、H661細胞具有顯著的毒殺活性,且能有效抑制肺癌細胞的轉移,因此BSE具有作為抗肺腺癌藥物之潛力。 Bulnesia sarmientoi tree, which mainly distributed in South America, is a slow-growing hardwood species. The traditional use of B. sarmientoi can eliminate wind, heat, and anti-toxic function, as well as to promote skin healing, appetizers, spleen function, and brain doping. Previous studies indicate that B. sarmientoi has anti-inflammatory and anti-cancer activities. The goal of this study is to investigate the anti-proliferation effects of B. sarmientoi supercritical fluid extract (BSE) against A549, H661, H1299 human lung cancer cells and normal embryonic lung fibroblast cells MRC-5 in vitro, and its necroptotic property. The experimental results showed that the IC50 are 43.7, 44.6 and 53.3 μg/ml, repectively, for A549, H661 and H1299 cells under 48 hr treatment of BSE. In comparison, the IC50 is 89.7 μg/ml for MRC-5 normal cells. This implies that BSE has the cytototic specificity on the cancer cells. Additionally, a positive correlation existed between the treatment time and the inhibition of cell growth, indicating that BSE is a long-duration type of tumor suppressor agent. The flow cytometric analysis indicated that BSE could arrest cancer cells in G2/M phase of the cell cycle. Furthermore, the necroptotic effect of BSE on A549 and H661 cells was confirmed by annexin V-FITC/PI double staining. BSE induced lung cancer cells to the necroptosis pathway was further verified by Western blot analysis, since the pro-necroptotic TNF-α, RIP-1 and RIP-3 proteins were down-regulated and the anti- necroptotic caspase-8 was up-regulated. From the assays of wound healing, migration and invasion, BSE was proved to have a significant inhibitory activity on the migration of lung cancer cells. The results of Western blot analysis showed that the BSE treatment down-regulated the expression of MMP-2 and MMP-9. Taken together, since BSE possesses significant cytotoxicity on A549 and H661 cells and inhibitory activity on the metastasis of lung cancer cells, it may serve as a potential target for the treatment of lung cancer.
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310002720236 博碩士論文區(二樓) 不外借資料 學位論文 TH 008M/0019 420208 1195 2014 一般使用(Normal) 在架 0
310002720244 博碩士論文區(二樓) 不外借資料 學位論文 TH 008M/0019 420208 1195 2014 c.2 一般使用(Normal) 在架 0
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