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題 名 | 鼠尾草酸對人類神經母細胞瘤IMR-32細胞株細胞週期之影響=Effect of Carnosic Acid on the Induction of Cell Cycle Arrest in Human Neuroblastoma IMR-32 Cells |
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作 者 | 林家媛; 蔡佳文; | 書刊名 | 臺灣營養學會雜誌 |
卷 期 | 36:4 2011.12[民100.12] |
頁 次 | 頁116-124 |
分類號 | 411.38 |
關鍵詞 | 鼠尾草酸; 活性氧化物質; 細胞週期; p38激酶; 人類神經母細胞瘤IMR-32細胞株; Carnosic acid; Reactive oxygen species; Cell cycle; p38 kinase; Human neuroblastoma IMR-32 cells; |
語 文 | 中文(Chinese) |
中文摘要 | 鼠尾草酸(carnosic acid, CA)為迷迭香中的二萜類(diterpene),由於我們先前的研究發現CA會透過增加活性氧化物質(reactive oxygen species, ROS)而活化p38蛋白,以促進人類神經母細胞瘤(neuroblastoma)IMR-32細胞發生凋亡。因此,本研究欲探討CA減少IMR-32細胞生長是否與ROS和p38路徑影響其細胞週期有關。IMR-32細胞以30 μM的CA處理12-60小時,流式細胞儀結果顯示在CA處理24小時後,細胞滯留在GO/G1期的比例顯著地增加,而且CA隨處理濃度的增加而降低週期素(cyclins)中的cyclin D1和cyclinD3以及週期素激酶(cyclin-dependent kinases, CDKs)中的CDK4和CDK6蛋白表現,然而CA對於細胞週期抑制性蛋白(cyclin dependent kinase inhibitors, CDKls)中p21蛋白的表現卻隨著濃度的增加而增加。另外,細胞若先處理抗氧化劑N-乙醯基半胱氯酸(N-acetylcysteine,NAC)或進行p38 siRNA實驗,則會抑制CA增加p21蛋白的能力,並回復CA抑制CDK4蛋白的能力。結論:CA可能透過調節p21和CDK4蛋白表現,使IMR-32細胞停滯在GO/G1期,且此路徑可能與ROS和p38路徑有關,因此,CA未來可能可發展為抵抗神經母細胞瘤的化學預防治療策略。 |
英文摘要 | Carnosic acid (CA) is a phenolic diterpene obtained from rosemary (Rosmarinus officinalis) . Our previous study indicated that CA induced apoptotic cell death through reactive oxygen species (ROS) -mediated phosphorylation of p38 in human neuroblastoma IMR-32 cells. In this study, we explored whether CA-reduced cell viability was associated with cell-cycle arrest through ROS generation and the p38 pathway. IMR-32 cells were treated with 30 μM CA for 12~60 h. A flow cytometric analysis indicated that cells were significantly arrested in the GO/G1 phase when treated with CA for 24 h (p < 0.05). Immunoblotting suggested that CA decreased the levels of cell-cycle regulatory proteins such as cyclin D1, cyclin D3, CDK4, and CDK6 proteins, while increasing the level of p21 protein. Pretreatment with the antioxidant, N-acetylcysteine (NAC), or p38 siRNA inhibited CAinduced p21 expression, whereas it reversed CA-decreased CDK4 expression. In conclusion, CA induced ROS generation and p38 activation, which in turn modulated the protein expressions of p21 and CDK4, and induced GO/G1 cell-cycle arrest in IMR-32 cells. Therefore, CA has the potential to be developed as a therapeutic agent against neuroblastoma. |
本系統中英文摘要資訊取自各篇刊載內容。