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標題: | 薑黃素抑制Nifedipine 經由活性氧化物誘導牙齦上皮細胞活化潛伏性TGF-β Nifedipine activated latent TGF-β through reactive oxygen species in gingival epithelial cells: Suppression by curcumin |
作者: | 胡瑋凡 Wei-Fan Hu |
指導教授: | 郭彥彬 Mark Yen-Ping Kuo |
關鍵字: | 尼菲迪平,牙齦過度增生,潛在的轉型生長因子,活性氧化物,上皮-間質細胞轉換, Nifedipine,Gingival overgrowth,Latent TGF-β,ROS,EMT, |
出版年 : | 2023 |
學位: | 碩士 |
摘要: | Nifedipine 是一種常用來治療高血壓的藥物,但使用此藥物時,常會導致病人牙齦過度增 生(Gingival overgrowth,GO),進而影響病人的說話、吞嚥、咀嚼、口腔衛生和外貌等基 本功能,使生活品質受到嚴重影響。目前治療 GO 的主要方法是手術切除,但復發率高。許 多研究指出,在腫瘤轉移和器官纖維化等疾病中,上皮-間質轉換(Epithelial-mesenchymal transition,EMT)是重要的生物學現象,而轉型生長因子-β(Transforming growth factor-β, TGF-β)是誘導EMT的重要因子。除此之外,其在牙齦過度生長、纖維化等疾病中也扮演著重要角色。本研究發現,在處理 Nifedipine 24 小時後,人類牙齦上皮 Ca9-22 細胞株會出 現 EMT 現象,其中 E-cadherin 的表現量下降,Slug 的表現量上升,並且以 TGF-β 的中和抗體前處理後,可以抑制 Nifedipine 誘導的 EMT。前處理抗氧化劑 N-acetyl-cystenine(ROS 抑 制劑)、Mito-TEMPO(粒線體 ROS 抑制劑)、Diphenylene iodonium(NOX 抑制劑)、 Plumbagin(NOX4 抑制劑)、Apocynine(NOX2 抑制劑)可以抑制 Nifedipine 誘導的活化 態 TGF-β 的產生。而常見的天然食品成分薑黃素(Curcumin)可以抑制 Ca9-22 細胞中 Nifedipine 誘導的活化態 TGF-β 的釋放,進而抑制 TGF-β 下游的訊息傳遞。這些發現有助於 未來開發治療或預防 GO 的潛力藥物,例如薑黃素等。 Nifedipine is a commonly used medication to treat hypertension, but its use often leads to gingival overgrowth (GO) in patients, which affects their basic functions such as speaking, swallowing, chewing, oral hygiene, and appearance, thus seriously impacting their quality of life. Currently, the main method to treat GO is surgical removal, but the recurrence rate is high. Many studies have pointed out that epithelial-mesenchymal transition (EMT) is an important biological phenomenon in diseases such as tumor metastasis and organ fibrosis, and transforming growth factor-β (TGF-β) is an important factor inducing EMT. In addition, it also plays an important role in diseases such as gingival overgrowth and fibrosis. This study found that after treating with Nifedipine for 24 hours, human gingival epithelial Ca9-22 cells exhibited EMT, with a decrease in the expression of Ecadherin and an increase in the expression of Slug. Further experiments showed that Nifedipine can induce the TGF-β signaling pathway, and pre-treatment with antioxidants such as N-acetylcystenine (ROS inhibitor), Mito-TEMPO(Mitochondria-targeted O 2 - inhibitor), Diphenylene iodonium (NOX inhibitor), Plumbagin (NOX4 inhibitor), and Apocynine (NOX2 inhibitor) can inhibit the production of activated TGF-β induced by nifedipine. The common natural food ingredient, curcumin, can inhibit the release of activated TGF-β induced by Nifedipine in Ca9-22 cells, thereby inhibiting downstream signaling of TGF-β. These findings may contribute to the development of potential drugs for treating or preventing GO, such as curcumin. |
URI: | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/89637 |
DOI: | 10.6342/NTU202301460 |
全文授權: | 未授權 |
顯示於系所單位: | 臨床牙醫學研究所 |
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