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研究生:高英賢
研究生(外文):Ying-Hsien Kao
論文名稱:砷化鈉對培養人類臍靜脈血管內皮細胞之生物效應
論文名稱(外文):Biological effects of sodium arsenite on cultured human umbilical vein endothelial cells
指導教授:余幸司余幸司引用關係
指導教授(外文):Hsin-Su Yu
學位類別:碩士
校院名稱:高雄醫學大學
系所名稱:醫學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2001
畢業學年度:89
語文別:中文
中文關鍵詞:砷化鈉血管內皮細胞血管新生一氧化氮合成酉每血管內皮細胞生長因子
外文關鍵詞:sodium arsenitevascular endothelial cellsangiogenesisnitric oxide synthasevascular endothelial growth factor
相關次數:
  • 被引用被引用:2
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  • 下載下載:18
  • 收藏至我的研究室書目清單書目收藏:1
砷元素廣佈於自然界中,常經由工業的製造處理過程與農業用藥劑的使用,例如銅、鋅、鉛礦的冶煉、玻璃的製造、與化學製藥的過程將其濃縮後排放至環境之中。因此飲用水被砷物質所污染一直是個重要的公共衛生問題。世界各國均曾報導經由飲用水所造成急性或慢性的砷暴露;特別是在阿根廷、孟加拉、印度、墨西哥、泰國以及臺灣,在當地有大部份的飲用水(地下水)含有高濃度的砷物質。有足夠的流行病學研究證據指出砷暴露對一般健康的影響主要是使得罹患心臟與周邊血管疾病的机率增高,例如動脈血管粥狀硬化;砷物質會對血管壁造成退化性病變如烏腳病;砷暴露亦會造成細胞增生,目前已知與癌症的發生有極度的關聯性,在許多砷污染地區民眾罹患膀胱癌、腎臟癌、皮膚癌、肝癌與直腸癌的比例明顯地較一般地區為高。砷暴露對其他系統的危害有胎兒發育異常、神經行為異常、肝臟門脈纖維化、肺部纖維化等。本研究的目的在探討砷物質是否對血管內皮細胞的生長與生理病理功能具有調控作用,特別是針對血管內皮細胞的增殖性與另一特殊分化功能 - 血管新生 (angiogenesis) - 作一初步的觀察。研究結果顯示砷化鈉對培養人類血管內皮細胞的生長及其他生物效應均具有典型的雙相(biphasic)效應。研究指出低於1 M的砷化鈉可促進細胞的增殖性。In vitro angiogenesis的觀察結果顯示低濃度(<1 M)之砷化鈉可剌激血管內皮細胞血管新生的發生,而高濃度砷化鈉的處理則明顯地呈現毒性抑制作用。我們亦發現砷化鈉除了會增加一氧化氮合成脢(NOS)基因與蛋白質表現外,亦可調節VEGF基因與蛋白質的表現,以及促進von Willebrand Factor(vWF)蛋白的表現。vWF被認為是一可用來作為評估腫瘤組織中血管內皮層活化狀態的指標,其可反應出腫瘤轉移初期angiogenesis發生的可能性,並且體外試驗已證實VEGF與bFGF這兩種angiogenic factors可協同性地刺激vWF的表現。因此低濃度砷化鈉的處理能導致血管內皮細胞的增生與活化,較利於誘發及維持angiogenesis的發生。然而,砷物質可促進血管新生發生的分子機轉仍有待進一步研究。
Arsenic is widely distributed in nature and frequently concentrated and released into the environment through industrial processes and agricultural usage such as primary copper, zinc and lead smelters, glass manufacturers, and chemical manufacturers. Drinking water contamination by arsenic remains a major public health problem. Acute and chronic arsenic exposure via drinking water has been reported in many countries of the world; especially in Argentina, Bangladesh, India, Mexico, Thailand, and Taiwan, where a large proportion of drinking water (ground water) is contaminated with a high concentration of arsenic. There were sufficient evidence from epidemiological studies to support a causal association between arsenic exposure and human diseases. General health effects that are associated with arsenic exposure include higher mortality ratio with cardiovascular disease such as atherosclerosis. Arsenic exposure also leads to degenerative peripheral vascular disease like blackfoot disease. In addition, research pointed out significantly higher standardized mortality ratios and cumulative mortality rates for cancers of the bladder, kidney, skin, liver, and colon in many areas of arsenic pollution. Others include developmental anomalies, neurologic and neurobehavioral disorders, portal fibrosis of the liver, and lung fibrosis. The purpose of this study was to investigate whether arsenic participates in the regulation of cell proliferation and other patho- and physiologic functions in vascular endothelial cells, and particularly focused on angiogenesis - one form of differentiation specific to endothelial cells. The results revealed that sodium arsenite (SA) exhibits typical biphasic biological effects on cell growth. Lower concentration (up to 1 M) of SA stimulates HUVEC proliferation. Similarly, in vitro angiogenesis assay indicated that low concentrations of SA maintain the morphogenesis of vascular tubular formation, whereas high concentration of SA revealed cytotoxic inhibition. We also demonstrated that lower concentration of SA can upregulate the expression of constitutive nitric oxide synthase (eNOS) at both transcriptional and translational levels, and that lower concentration of SA implicated a modulatory role in VEGF expression. Additionally, lower concentration of SA (<1 M) could stimulate the vWF antigen expression. vWF was demonstrated to be an indicator of representing the activation of endothelium in tumor tissue, which paralleled with the onset of angiogenesis preceding the tumor metastasis. In vitro study also demonstrated that two angiogenic factors, VEGF and bFGF, can synergistically upregulate the vWF gene expression. Therefore, we conclude that the treatment of HUVEC with SA leads to the cell proliferation and activation, which preferentially enhances the angiogenesis in vitro. The molecular mechanism(s) by which arsenic facilitates angiogenesis, however, remain to be elucidated.
二、 英文摘要……………………………… 3
三、 英文縮寫……………………………… 5
四、 前 言……………………………… 8
五、 材料與方法…………………………… 20
六、 研究結果……………………………… 32
七、 討 論……………………………… 36
八、 結論與展望…………………………… 39
九、 參考文獻……………………………… 40
十、 圖 表……………………………… 54
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