本文選題：褐藻多糖硫酸酯　切入點：淋巴道轉(zhuǎn)移　出處：《大連醫(yī)科大學(xué)》2015年碩士論文　論文類型：學(xué)位論文

【摘要】：目的：腫瘤轉(zhuǎn)移是惡性腫瘤的基本特征和重要標(biāo)志,腫瘤轉(zhuǎn)移是一個多因素,多步驟,多基因共同調(diào)控的復(fù)雜過程,涉及大量相關(guān)基因結(jié)構(gòu)和表達(dá)調(diào)控的改變,腫瘤發(fā)生轉(zhuǎn)移與腫瘤細(xì)胞增殖、粘附、降解細(xì)胞外基質(zhì)、侵襲、遷移密切相關(guān)。多糖是一類天然高分子產(chǎn)物,廣泛存在于動物細(xì)胞膜、植物和微生物細(xì)胞壁中,具有多重功效,且毒副作用小。褐藻多糖硫酸酯(Fucoidan)是一類富含L-巖藻糖和硫酸基團(tuán)的雜多糖,存在于海洋褐藻和棘皮動物體內(nèi),具有免疫調(diào)節(jié)、抗腫瘤i降血、抗衰老等生物活性。其中Fucoidan抗腫瘤活性成為多糖抗腫瘤研究的熱點。小鼠肝癌Hca-F和Hca-P細(xì)胞系是我校病理學(xué)教研室凌茂英教授從近交系昆明小鼠腹水型肝癌細(xì)胞H22中篩選建系,其中Hca-F細(xì)胞淋巴道轉(zhuǎn)移率高達(dá)70%,Hca-P細(xì)胞則低于30%,是研究腫瘤淋巴道轉(zhuǎn)移經(jīng)典細(xì)胞模型。血管內(nèi)皮生長因子-C (VEGF-C)與腫瘤細(xì)胞生長、增殖、轉(zhuǎn)移密切相關(guān),VEGFR-3是VEGF-C特異性受體,在某些腫瘤細(xì)胞中有表達(dá)。本課題組前期研究表明VEGFR-3在Hca-F細(xì)胞中有表達(dá)。VEGF-C與VEGFR-3結(jié)合,可上調(diào)肝細(xì)胞生長因子(HGF)表達(dá),激活下游信號通路,調(diào)控腫瘤的增殖、侵襲轉(zhuǎn)移。腫瘤轉(zhuǎn)移主要分為血道轉(zhuǎn)移和淋巴道轉(zhuǎn)移,淋巴道轉(zhuǎn)移是惡性腫瘤早期發(fā)生發(fā)展的關(guān)鍵。腫瘤轉(zhuǎn)移首先需要腫瘤細(xì)胞自身增殖,進(jìn)而發(fā)生粘附,然后降解細(xì)胞外基質(zhì),從而發(fā)生轉(zhuǎn)移�；|(zhì)金屬蛋白酶家族(MMPs)是降解細(xì)胞外基質(zhì)的主要成員,在促進(jìn)腫瘤轉(zhuǎn)移過程中具有重要作用,而基質(zhì)金屬蛋白酶組織抑制劑(TIMPs)可以抑制MMPs活性,抑制腫瘤細(xì)胞轉(zhuǎn)移能力。本研究以小鼠肝癌Hca-F細(xì)胞為細(xì)胞模型,采用細(xì)胞生物學(xué),生物化學(xué)以及分子生物學(xué)等方法,探究N-Fucoidan對Hca-F細(xì)胞生長、轉(zhuǎn)移、侵襲能力的改變進(jìn)而探究N-Fucoidan抑制腫瘤轉(zhuǎn)移的分子機(jī)制。方法：1.采用乙醇分級沉淀法從粗品Fucoidan中純化獲得N-Fucoidan,使用過氧化氫抗壞血酸聯(lián)合作用法降解N-Fucoidan,乙醇沉淀后獲得LMW-Fucoidan.2.采用苯酚-硫酸法、氯化鋇明膠比濁法、硫酸-咔唑法、自動指示旋光儀、核磁共振儀分別測定N-Fucoidan與LMW-Fucoidan的總糖含量、硫酸根含量、糖醛酸含量、旋光度和官能團(tuán)。3.采用MTT法,Transwell法,Elisa雙抗夾心法比較Hca-P細(xì)胞和Hca-F細(xì)胞生長、侵襲能力、生長因子和MMPs分泌的差異。4.通過臺盼藍(lán)染色法檢測N-Fucoidan對Hca-F細(xì)胞毒作用,并計算存活率。5.MTT法檢測N-Fucoidan對Hca-F細(xì)胞生長能力的影響,采用Transwell實驗檢測N-Fucoidan對Hca-F細(xì)胞侵襲能力的影響。6. Western blot法檢測經(jīng)過N-Fucoidan處理后Hca-F細(xì)胞后,細(xì)胞總蛋白中VEGFR-3, C-MET,CXCR-4, TIMP-1蛋白水平表達(dá)的影響,并通過ELISA法檢測細(xì)胞上清中MMP-2、MMP-9、VEGF-C和HGF分泌能力的變化,RT-PCR檢測vegf-c, c-met, timp-1相關(guān)基因mRNA表達(dá)水平的影響。7.MTT法比較N-Fucoidan和LMW-Fucoidan對Hca-F細(xì)胞生長能力的影響,ELISA法比對N-Fucoidan和LMW-Fucoidan對VEGF-C、HGF、MMP-2、MMP-9表達(dá)水平的不同,Western blot法檢測N-Fucoidan和LMW-Fucoidan處理Hca-F細(xì)胞后總蛋白中VEGFR-3, C-MET,CXCR-4, TIMP-1蛋白水平表達(dá)的影響。8.采用經(jīng)典淋巴道轉(zhuǎn)移模型,對615小鼠足墊接種Hca-F細(xì)胞,N-Fucoidan對體內(nèi)腫瘤轉(zhuǎn)移的影響。通過ELISA法檢測血清中VEGF-C, HGF的含量,HE染色法觀察形態(tài)變化,免疫組化法檢測淋巴管密度。9.采用不完全弗式佐劑誘導(dǎo)mLEC, MTT法檢測N-Fucoidan對mLEC細(xì)胞增殖能力的影響,免疫熒光法鑒定]mLEC細(xì)胞中LYVE-1蛋白的表達(dá),鏡下觀察N-Fucoidan對]mLEC成管的影響。結(jié)果：1. N-Fucoidan的得率為38.91%,從純化的N-Fucoidan采用過氧化氫-抗壞血酸法降解得到LMW-Fucoidan的得率為60%2. N-Fucoidan總糖含量、硫酸基團(tuán)含量、糖醛酸含量分別為44.7%、18.5%、12.5%。LMW-Fucoidan總糖含量為48.7%,硫酸基團(tuán)含量為14.5%、糖醛酸含量為16.5%。3.實驗結(jié)果表明,Hca-F細(xì)胞生長能力是Hca-P細(xì)胞的1.79倍,Hca-F細(xì)胞侵襲能力是Hca-P細(xì)胞的1.67倍,Hca-F細(xì)胞分泌VEGF-C、HGF、MMP-2、MMP-9能力分別是Hca-P細(xì)胞分泌能力的1.09倍、1.03倍、1.21倍、1.25倍。4. N-Fucoidan處理Hca-F細(xì)胞后,細(xì)胞死亡率小于1%,表明Fucoidan抑制Hca-F細(xì)胞增殖并非細(xì)胞毒作用。5.實驗結(jié)果顯示經(jīng)過N-Fucoidan處理后細(xì)胞生長能力收到抑制呈藥物濃度及作用時間依賴性關(guān)系。Transwell實驗結(jié)果顯示,N-Fucoidan抑制Hca-F細(xì)胞發(fā)生細(xì)胞侵襲,呈時間劑量依賴性關(guān)系。6.實驗結(jié)果表明,N-Fucoidan處理Hca-F細(xì)胞后,細(xì)胞總蛋白中VEGFR-3、 C-MET、CXCR-4蛋白表達(dá)受到抑制,TIMP-1的表達(dá)能力被激活。ELISA結(jié)果顯示；經(jīng)過N-Fucoidan處理后,N-Fucoidan抑制細(xì)胞分泌MMP-2、MMP-9、VEGF-C、 HGF、SDF-1相關(guān)生長因子,vegf-c、c-met、vegfr-3相關(guān)基因mRNA水平表達(dá)下調(diào),timp-1的表達(dá)上調(diào)。7.實驗結(jié)果表明LMW-Fucoidan比N-Fucoidan對Hca-F細(xì)胞生長具有更強的抑制作用。ELISA結(jié)果顯示經(jīng)過藥物處理后,Hca-F細(xì)胞分泌MMP-2、MMP-9、 VEGF-C、HGF水平及mRNA水平均下調(diào),N-Fucoidan效果強于LMW-Fucoidan。8. N-Fucoidan能夠抑制腫瘤細(xì)胞生長,增加小鼠脾臟指數(shù)和胸腺指數(shù),血清中VEGF-C和HGF的含量下降,腫瘤組織淋巴管密度降低。9.mLEC誘導(dǎo)成功,LYVE-1陽性細(xì)胞數(shù)大于85%, N-Fucoidan對mLEC生長有抑制作用,呈濃度依賴關(guān)系。結(jié)論：N-Fucoidan和LMW-Fucoidan對Hca-F細(xì)胞生長、侵襲和轉(zhuǎn)移能力均有抑制作用。N-Fucoidan的抑制作用機(jī)制與降低MMP-2, MMP-9活性,鈍化VEGF-C/VEGFR-3, HGF/C-MET, SDF-1/CXCR-4信號軸通路,降低腫瘤細(xì)胞活性及轉(zhuǎn)移能力。
[Abstract]:Objective: tumor metastasis is the basic characteristic of malignant tumor and tumor metastasis is an important symbol of a multi factor, multi steps, complex process regulated many genes, involving a large number of genes changed in structure and expression, metastasis and tumor cell proliferation, tumor adhesion, extracellular matrix degradation, invasion, migration and close. Polysaccharide is a kind of natural polymer product, widely exists in animal cell membranes, plants and microorganisms in the cell wall, has multiple effects and low toxicity. Fucoidan (Fucoidan) is a kind of rich in L- fucose and sulfate radical polysaccharide in marine brown algae and spine the animal skin, have immunomodulatory, antitumor I blood, anti-aging bioactivities. The antitumor activity of Fucoidan has become a hot study of antitumor polysaccharide. Mouse Hca-F and Hca-P cells, is our school Department of Pathology Professor Ling Maoying from Kunming inbred mouse ascites hepatoma cell line H22 screening, including Hca-F cell lymphatic metastasis rate is as high as 70%, Hca-P cells were less than 30%, is the study of lymphatic metastasis of tumor cells. The classical model of vascular endothelial growth factor -C (VEGF-C) and tumor growth, cell proliferation, metastasis VEGFR-3, VEGF-C is the specific receptor, in some tumor cells to express. Previous study showed that the expression of VEGFR-3.VEGF-C combined with VEGFR-3 in Hca-F cells, regulation of hepatocyte growth factor (HGF) expression and activation of downstream signaling pathways, regulation of tumor cell proliferation, invasion and metastasis. Tumor metastasis is mainly divided into the blood and lymph node metastasis, lymph node metastasis of malignant tumor is the key to early occurrence and development of tumor metastasis. First tumor cell proliferation, adhesion and degradation of extracellular matrix, and then, from And the occurrence of metastasis. Matrix metalloproteinases (MMPs) is a leading member of the degradation of extracellular matrix, which plays an important role in the process of promoting tumor metastasis, and tissue inhibitor of matrix metalloproteinase (TIMPs) can inhibit the activity of MMPs, inhibit the metastasis of tumor cells. In this study, mouse liver cancer Hca-F cell by cell biology, biochemistry and molecular biology methods, exploring the N-Fucoidan growth, metastasis of Hca-F cells, molecular mechanism of invasion ability changes and explore the N-Fucoidan inhibition of tumor metastasis. Methods: 1. using ethanol precipitation method from crude and purified Fucoidan in N-Fucoidan, the combined effects of the use of hydrogen peroxide ascorbic acid degradation by N-Fucoidan, ethanol precipitation obtained by LMW-Fucoidan.2. phenol sulfuric acid method, barium chloride gelatin nephelometry carzapol sulfuric acid method, indicating automatic polarimeter, NMR The total sugar content were measured by N-Fucoidan and LMW-Fucoidan NMR, sulfate content, uronic acid content, rotation and.3. groups with MTT method, Transwell method, Elisa double sandwich method between Hca-P cells and Hca-F cell growth, invasion, growth difference factor and MMPs secretion of.4. was detected by trypan N-Fucoidan on Hca-F the cytotoxic effect of blue staining, and calculate the influence survival rate of.5.MTT N-Fucoidan was detected on the proliferation of Hca-F cells were detected by Transwell, the influence of N-Fucoidan on the invasion ability of Hca-F cells.6. Western blot assay after treatment with N-Fucoidan in Hca-F cells, VEGFR-3 cells, total protein in C-MET, CXCR-4, TIMP-1 protein expression level and, by MMP-2, the cell supernatant was detected by ELISA MMP-9, VEGF-C and HGF changes in the secretion of RT-PCR, c-Met, TIMP-1, VEGF-C detection, mRNA gene expression Effect of.7.MTT N-Fucoidan and LMW-Fucoidan flat effect on growth of Hca-F cells, ELISA N-Fucoidan and LMW-Fucoidan method comparison of VEGF-C, HGF, MMP-2, MMP-9 different levels of expression, Western blot method to detect N-Fucoidan and LMW-Fucoidan protein in Hca-F cells after treatment of total VEGFR-3, C-MET, CXCR-4,.8. expression level of TIMP-1 protein by the classic model of lymphatic metastasis, the 615 foot pads of mice inoculated with Hca-F cells, the effect of N-Fucoidan on tumor metastasis. Serum ELISA was detected by VEGF-C method, the content of HGF, observe the morphological changes of HE staining, immunohistochemical detection of lymphatic microvessel density.9. with complete Freund's adjuvant induced mLEC effect detection of N-Fucoidan MTT methods the proliferation of mLEC cells, the expression of LYVE-1 protein by fluorescence method in identification of]mLEC cells, N-Fucoidan tube effect on]mLEC was observed under microscope: 1. N-Fucoidan was 38.91%. The purified N-Fucoidan using hydrogen peroxide ascorbic acid degradation by LMW-Fucoidan was 60%2. N-Fucoidan total sugar content, sulfate content and uronic acid content were 44.7%, 18.5%, the total sugar content of 12.5%.LMW-Fucoidan is 48.7%, the sulfate content was 14.5%, uronic acid content is 16.5%.3. the experimental results show that Hca-F, cell growth ability is 1.79 times that of Hca-P cells, Hca-F cell invasion ability is 1.67 times that of Hca-P cells, Hca-F cells secrete VEGF-C, HGF, MMP-2, MMP-9 were 1.09 times, Hca-P cells secreting capacity of 1.03 times, 1.21 times, 1.25 times.4. N-Fucoidan after treatment of Hca-F cells, cell death rate is less than 1% that showed that Fucoidan inhibited the proliferation of Hca-F cells is not the cytotoxic effect of.5. experimental results showed that after treatment with N-Fucoidan inhibited cell growth ability in drug concentration and action time Dependence of the.Transwell results showed that N-Fucoidan inhibited cell invasion of Hca-F cells in a time dose dependent relationship between the.6. and the experimental results show that N-Fucoidan after treatment of Hca-F cells, VEGFR-3 cells, total protein C-MET, CXCR-4 protein expression was inhibited, the expression ability of TIMP-1 activated by.ELISA results; after N-Fucoidan treatment, the inhibition of N-Fucoidan the secretion of MMP-2 cells, MMP-9, VEGF-C, HGF, SDF-1 VEGF-C, c-Met, growth factor, VEGFR-3 related gene mRNA expression level of TIMP-1, while the expression of.7. test results showed that the inhibitory effect of.ELISA LMW-Fucoidan is stronger than N-Fucoidan on the growth of Hca-F cells showed that after drug treatment, Hca-F cells secrete MMP-2, MMP-9, VEGF-C HGF, and mRNA level declined, N-Fucoidan is better than LMW-Fucoidan.8. N-Fucoidan can inhibit the growth of tumor cells, Increase the spleen index and thymus index of mice, decreased the contents of VEGF-C and HGF in serum, tumor lymphatic density decreased.9.mLEC induced successfully, the number of LYVE-1 positive cells was greater than 85%, N-Fucoidan inhibited the proliferation of mLEC cells in a dose-dependent manner. Conclusion: N-Fucoidan and LMW-Fucoidan on the growth of Hca-F cells, the mechanism of inhibition of invasion and metastasis have the inhibitory effect of.N-Fucoidan and MMP-2 decreased, the activity of MMP-9, VEGF-C/VEGFR-3 HGF/C-MET, SDF-1/CXCR-4 passivation, signal pathway, reduce the activity of tumor cells and metastasis.

【學(xué)位授予單位】：大連醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2015
【分類號】：R73-3

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