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標題: | 遠紅外線對肝癌的影響 The effect of Far-infrared radiation (FIR) in Human Hepatocellular carcinoma |
作者: | Ching-Feng Lin 林敬峰 |
指導教授: | 陳兆勛(Chau-Hsun Chen) |
關鍵字: | 肝癌,Hep3B,FIR,細胞凋亡,轉移,Caspase3,Bax,Bcl-2,MMP9,COX-2,非熱效應, HHC,Hep3B,FIR,Apoptosis,Migration,Bax,Bcl-2,Caspase3,MMP9,COX-2, |
出版年 : | 2014 |
學位: | 碩士 |
摘要: | 肝癌是全世界最普遍的癌症之一,在台灣也常常冠居全台年癌症致死率最高之首。在眾多治療癌症的方法中,仍是以抗癌藥物的開發為最有效的治療方法。至今仍然沒有一個有效的非藥物性治療方法。是故尋找一個非藥物性的治療是我們的目的。遠紅外線為一波長介於4~1000微米之不可見光,其照射人體後所產生之熱效應與非熱效應在醫學物理治療上已被廣泛的討論。非熱效應在中醫的理論中被視為氣,也就是能量的表現。近年來遠紅外線也在西方醫療中逐漸被重視,除了已經被證實在人體內膜的發炎表現途徑中能夠透過誘導血紅素加氧酶-1(HO-1)表現進而抑制血管發炎,亦在口腔癌跟齒齦癌的研究上證實經由遠紅外線之非熱效應照射後其癌細胞的增生明顯被抑制。本實驗之目的是希望藉由Morphology assay、Migration assay、Wound healing assay、Western blot、Zymography了解肝癌細胞在受到遠紅外線照射後之細胞凋亡、轉移、增生的變化,並且探討非熱效應。由Morphology assay了解到細胞萎縮、凋亡的現象,並且由Migration assay 與Wound healing assay了解到細胞轉移、爬行的能力與增生能力的下降。由Bax蛋白的上調與Bcl-2蛋白的下調我們了解FIR或許能夠透過粒線體凋亡的途徑誘導Hep3B凋亡,並由Caspase3蛋白的表現應證凋亡途徑的產生。環氧合酶-2(Cyclooxygenase-2;COX-2)與基質金屬蛋白酶(Matrix metallo proteinases;MMPs)是癌症轉移及發炎反應、血管增生、細胞增生過程中主要參與的蛋白。在現行的抗癌藥物開發中COX-2抑制劑與MMP-9抑制劑已是治療癌症的標把藥物。透過Western blot我們發現癌細胞Hep3B在經過遠紅外線照射後其COX-2蛋白與MMP9蛋白的活性明顯的被抑制,且證實非熱效應參與了其中之調控。這樣的結果是遠紅外線能夠抑制癌細胞的生長強而有力的證據。未來是否能夠做為一個抑制肝癌的物理性治療,進一步做活體動物實驗與配合藥物做複合式的實驗使治療達到效率最佳化化,都是未來可以研究的方向。 Human Hepatocellular carcinoma(HHC) is one of the most common cancers in the world, it always got the highest fatality rate than any other cancers for decades in Taiwan. To increase the survival rate or reduce the fatality rate, it is necessary and important to find a way to do that, the invention of anti-cancer drugs is still considered a main way to heal HHC, there isn’t a physical treatment to be proved that can heal HHC in the world. Therefore, finding a sufficient physical way is our propose. The Far-infrared radiation(FIR) is used to being a physical treatment in Traditional Chinese Medicine(TCM) for a long time. It is getting attention Western Medicine in recent years. Not only is FIR being proved that can reduce angiogenesis in human body but also it can reduce the proliferation in tongue cancer and lung cancer by reducing HSP70 expression level. Our experiment is to show the effect of FIR in HHC. By Morphology assay、Migration assay、Wound healing assay ,we know that FIR can cause HHC to death and reduce the level of migration and proliferation. By overexpression level of Bax and inhibit expression level of Bcl-2,we know that FIR cause the crash of mitochondrial outer membrane permeabilization (MOMP) balance and induce apoptosis, and by the expression of Caspase 3 we can prove that apoptosis happened. By reducing the expression of COX-2 and MMP9, the outcome shows that FIR can inhibit migration of Hep3B,and also it can inhibit angiogenesis and proliferation. This is a sufficient evidence that FIR can reduce Hep3B in many ways. The effect of experiment FIR in mice or experiment FIR with anti-drugs can be foreseen for the Hep3B. |
URI: | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/18429 |
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顯示於系所單位: | 應用力學研究所 |
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