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    National Tsing Hua University Institutional Repository > 生命科學院  > 分子醫學研究所 > 博碩士論文 >  低劑量游離輻射促進海馬迴神經細胞中粒線體的融合


    Please use this identifier to cite or link to this item: http://nthur.lib.nthu.edu.tw/dspace/handle/987654321/85680


    Title: 低劑量游離輻射促進海馬迴神經細胞中粒線體的融合
    Authors: 劉思廷
    Liu, Szu-Ting
    Description: GH02101080550
    碩士
    分子醫學研究所
    Date: 2014
    Keywords: 放射線;低劑量;粒線體;粒線體融合;海馬迴神經細胞;乙型-澱粉樣蛋白
    radiation;low dose radiation;mitochondria;fusion;hippocampal neuron;beta-amyloid
    Abstract: 放射線治療在腫瘤治療上是一種十分常見的治療方式,主要是藉由傷害DNA的結構的方式,使得快速分裂增生的細胞死亡而達到腫瘤治療的目的。在臨床放射線治療中,會根據目標腫瘤組織的不同,劑量的選擇上會從1.8 Gy到20 Gy之間來做選擇,而在一般的情況下,2 Gy的劑量即可使得腫瘤細胞死亡。但在放射線治療的過程中,尤其是在腦部的腫瘤治療上,可能會由於放射線的治療,而影響腦部神經的發育,特別是與學習記憶最有關係的海馬迴神經細胞,另外,也有研究指出,在低劑量的放射線治療之下,會增加細胞的存活率和DNA修復,在我們的實驗中已經證實,利用MTT assays發現在低劑量(0.2 Gy)的放射線處理之下會增加細胞的活性,但不會增加細胞數,因此我們認為放射線或許會影響粒線體的活性,在實驗結果中可以明顯的發現,在0.2 Gy 的放射線處理之下,會使得粒線體融合並增長,以及Drp1的蛋白質表現量下降,證實粒線體會走向融合的路徑,但低劑量的放射線並不會增加粒線體的膜電位、氧化程度以及粒線體DNA的複製數目。最後,在我們研究中想了解放射線是否會對受損的神經達到治療的效果,阿茲海默症是常見的失智症之一,在阿茲海默症的病人中常可觀察到大腦中海馬迴受到損害,導致病人的學習記憶能力受損,因此我們使用beta-amyloid (Aβ)處理海馬迴神經細胞,模擬阿茲海默症中受到傷害的神經細胞,並且照射不同劑量的放射線,但在實驗結果中尚未發現放射線有治療的效果。
    Irradiation is a common treatment in tumor therapy. Radiation can cause DNA damage and death of proliferating cells. During clinical radiation therapy, the radiation dose could range from 1.8 to 20 Gy depending on targets. In the normal cases, 2 Gy-radiation treatment will cause cancer cell death. In the brain tissue, hippocampal neuron is not as sensitive to radiation. Some studies indicated the low dose radiation would induce cellular protective mechanism to promote cell survival and DNA repair. In our study, we demonstrate the low dose radiation would promote survival of hippocampal neurons based on MTT assays. 0.2 Gy radiation treatment had no effect on the cell number. We hypothesized to investigate the relationship between irradiation and mitochondrial function. However, radiation treatment did not affect membrane potential, ROS level and mitochondrial DNA copy number. Interestingly, the low dose radiation (0.2 Gy) may promote the mitochondria fusion found by immunofluorescence staining. The relative level of Drp1, a fission protein, was decreased after radiation treatment. Hippocampus is the region of the brain that suffers damage in Alzheimer's disease. To determine whether low dosage radiation would have beneficial effect on neurodegenerative disease, we treated hippocampal neuron with beta-amyloid (Aβ) to mimic Alzheimer's pathology followed by radiation therapy. Our results so far did not show protective effect of radiation on Aβ-treated hippocampal neurons.
    URI: http://nthur.lib.nthu.edu.tw/dspace/handle/987654321/85680
    Source: http://thesis.nthu.edu.tw/cgi-bin/gs/hugsweb.cgi?o=dnthucdr&i=sGH02101080550.id
    Appears in Collections:[分子醫學研究所] 博碩士論文

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