本文選題：肺支氣管上皮BEAS-2B細胞 + 亞砷酸鈉��； 參考：《福建醫(yī)科大學》2014年碩士論文

【摘要】：目的： 砷污染已經(jīng)成為全世界范圍內(nèi)受到廣泛關注的環(huán)境問題之一，慢性砷中毒對人體多器官系統(tǒng)功能均可造成危害，并引起肝癌、腎癌、肺癌、膀胱癌和皮膚癌。皮間質(zhì)轉(zhuǎn)化（Epithelial-mesenchymal Transition）與腫瘤細胞的生長、侵襲、遷移有重要關聯(lián)。炎癥在腫瘤微環(huán)境中有促腫瘤的作用，促進惡性細胞的生存和增殖。本文旨在探討炎癥因子在慢性砷誘導永生化人肺支氣管上皮細胞轉(zhuǎn)化的作用。 方法： 1.永生化人肺支氣管上皮細胞BEAS-2B經(jīng)0.25uM亞砷酸鈉暴露培養(yǎng)66天，并進行軟瓊脂集落形成實驗，挑取細胞克隆消化培養(yǎng)為轉(zhuǎn)化細胞；對照組BEAS-2B相同條件無亞砷酸鈉培養(yǎng)66天。 2. Westernblot檢測上皮細胞標志蛋白E-Cadherin、間質(zhì)細胞標志蛋白Vimentin表達。 3. Westernblot檢測炎性體蛋白AIM2、ASC、炎性體通路下游炎癥細胞因子IL-1β 4. Westernblot檢測炎癥因子HMGB1的表達。 結(jié)果： 1. BEAS-2B細胞經(jīng)慢性亞砷酸鈉暴露66天，克隆形成率為22.77%，，較對照組（3.06%）具有顯著差異（p0.01）。 2.慢性砷誘導轉(zhuǎn)化的BEAS-2B細胞，形態(tài)由上皮細胞的不規(guī)則多邊形變?yōu)樗笮巍?3.轉(zhuǎn)化的BEAS-2B細胞較對照組上皮細胞標志蛋白E-Cadherin表達減少、間質(zhì)細胞標志蛋白Vimentin表達增加。 4.轉(zhuǎn)化的BEAS-2B細胞較對照組炎性體蛋白AIM2、ASC表達減少，炎性體通路下游炎癥細胞因子IL-1β表達減少。 5.轉(zhuǎn)化的BEAS-2B細胞HMGB1表達增加。 結(jié)論： 1.慢性砷誘導的BEAS-2B細胞形態(tài)發(fā)生改變，克隆形成能力增強，細胞發(fā)生轉(zhuǎn)化。 2.炎性體蛋白表達減少在BEAS-2B轉(zhuǎn)化中起一定的促進作用。 3.轉(zhuǎn)化的BEAS-2B細胞HMGB1表達增加，提示細胞轉(zhuǎn)化與HMGB1表達增強有關。
[Abstract]:Objective: arsenic pollution has become one of the most important environmental problems all over the world. Chronic arsenic poisoning is harmful to the function of human multi-organ system, and can cause liver cancer, kidney cancer, lung cancer, bladder cancer and skin cancer. Epithelial-mesenchymal Transitionis associated with the growth, invasion and migration of tumor cells. Inflammation promotes the survival and proliferation of malignant cells in tumor microenvironment. The aim of this study was to investigate the role of inflammatory factors in chronic arsenic induced transformation of immortalized human lung bronchial epithelial cells. The immortalized human lung bronchial epithelial cells BEAS-2B were exposed to 0.25 UM sodium arsenite for 66 days, and the soft Agar colony formation test was carried out to select the cells for clone digestion and culture into transformed cells, while the control group BEAS-2B was cultured without sodium arsenite for 66 days under the same conditions. 2. The expression of E-Cadherin in epithelial cells and Vimentin in interstitial cells was detected by Western blot. Western blot was used to detect the inflammatory protein AIM2 and the inflammatory cytokine IL-1 尾 4 downstream of the inflammatory pathway. The expression of HMGB1 was detected by Western blot. Results: 1. When BEAS-2B cells were exposed to chronic sodium arsenite for 66 days, the clone formation rate was 22.77, which was significantly different from that of the control group (3.06). The morphology of BEAS-2B cells induced by chronic arsenic was changed from irregular polygon of epithelial cells to fusiform. The expression of E-Cadherin in the transformed BEAS-2B cells was lower than that in the control group, and the expression of Vimentin was increased in the stromal cells. Compared with the control group, the expression of AIM2 + ASC in BEAS-2B cells was lower than that in the control group, and the expression of IL-1 尾 was decreased in the downstream of inflammatory pathway. The expression of HMGB1 in transformed BEAS-2B cells was increased. Conclusion: 1. BEAS-2B cells induced by chronic arsenic had morphologic changes, enhanced clone formation and cell transformation. 2. 2. The decrease of inflammatory body protein expression in BEAS-2B transformation plays a certain role in promoting. 3. The expression of HMGB1 in transformed BEAS-2B cells was increased, which suggested that the expression of HMGB1 was related to the expression of HMGB1 in transformed BEAS-2B cells.
【學位授予單位】：福建醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2014
【分類號】：R114

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