本文選題：肺移植 + 自噬　； 參考：《南昌大學》2015年碩士論文

【摘要】：目的:建立大鼠原位異體肺移植模型,明確自噬相關蛋白Beclin-1在大鼠肺移植供肺缺血再灌注損傷中的表達,然后通過調控自噬,研究Beclin-1蛋白表達含量、細胞凋亡水平及肺功能指標的變化,揭示自噬作用對肺移植供肺I/R損傷及肺功能指標的影響。方法:建立大鼠原位左肺移植模型,分別于供肺灌注、冷缺血保存、移植后再灌注2小時、6小時、12小時獲取供肺標本;檢測供肺Beclin-1蛋白的表達、細胞凋亡及肺功能指標水平。通過調控自噬,分別用LPD液、3-MA+LPD液、雷帕霉素+LPD液灌注、冷缺血保存供肺6小時后行肺移植術,于前一部分得出的自噬水平峰值時間點再灌后獲取供肺,再次檢測供肺Beclin-1蛋白的表達、細胞凋亡及肺功能指標水平。結果:1、建立了穩(wěn)定的大鼠原位肺移植模型。2、Beclin-1蛋白的表達在供肺缺血后逐漸上升,在再灌注6h達到高峰,供肺組織細胞凋亡水平及肺功能損傷指標在SD大鼠供肺灌注、冷缺血、再灌注后6h所獲取的肺標本中達到峰值。3、在3-MA+LPD液組Beclin-1蛋白的表達及細胞凋亡水平明顯降低,肺功能損傷減輕。雷帕霉素+LPD液組Beclin-1蛋白的表達及細胞凋亡水平明顯升高,肺功能損傷加重。結論:1、肺移植供肺缺血再灌注后,自噬相關蛋白Beclin-1及細胞凋亡水平升高,并在術后6h達到高峰。2、通過抑制自噬,自噬相關蛋白Beclin-1表達降低,細胞凋亡水平減輕,減輕肺功能損傷。抑制自噬對肺移植缺血再灌注損傷具有保護作用。3、通過激活自噬,自噬相關蛋白Beclin-1表達升高,細胞凋亡水平加重,加重肺功能損傷。激活自噬對肺移植缺血再灌注損傷具有促進作用。4、自噬在大鼠肺移植缺血再灌注損傷中可能起到了促進作用。
[Abstract]:Objective: to establish a rat model of orthotopic lung transplantation and to investigate the expression of autophagy associated protein (Beclin-1) in ischemia-reperfusion injury of donor lung in rats, and then to study the expression of Beclin-1 protein by regulating autophagy. The changes of apoptosis level and lung function index revealed the effect of autophagy on I / R injury and lung function index of donor lung transplantation. Methods: the model of orthotopic left lung transplantation was established in rats. Donor lung samples were obtained from donor lung perfusion, cold ischemia preservation and reperfusion for 2 hours, 6 hours and 12 hours, respectively, and the expression of Beclin-1 protein, apoptosis and lung function index were detected. By regulating autophagy, the donor lung was obtained after lung transplantation after 6 hours of cold ischemia preservation with LPD solution 3-MA LPD solution and rapamycin LPD solution, and the donor lung was obtained after reperfusion at the peak time point of autophagy level obtained in the first part of the experiment. The expression of Beclin-1 protein, apoptosis and lung function were detected again. Results the stable rat model of orthotopic lung transplantation was established. The expression of Beclin-1 protein increased gradually after ischemia of donor lung and reached its peak at 6 h after reperfusion. The level of apoptosis of donor lung tissue and the index of lung function injury were perfused into donor lung and cold ischemia in SD rats. The lung samples obtained 6 hours after reperfusion reached the peak value of .3. the expression of Beclin-1 protein and the level of apoptosis in the 3-MA LPD fluid group were significantly decreased, and the lung function injury was alleviated. In rapamycin LPD solution group, the expression of Beclin-1 protein and the level of apoptosis were significantly increased, and the lung function injury was aggravated. Conclusion the levels of autophagy associated protein (Beclin-1) and apoptosis in lung grafts increased after ischemia reperfusion and reached a peak at 6 h after lung transplantation. By inhibiting autophagy, the expression of autophagy associated protein Beclin-1 decreased and the level of apoptosis decreased. Reduce lung function injury. Inhibition of autophagy has a protective effect on ischemia-reperfusion injury of lung transplantation. By activating autophagy, the expression of autophagy associated protein Beclin-1 is increased, the level of apoptosis is aggravated, and the injury of lung function is aggravated. Activation of autophagy can promote ischemia-reperfusion injury of lung transplantation. 4. Autophagy may play a role in promoting ischemia-reperfusion injury of lung transplantation in rats.
【學位授予單位】：南昌大學
【學位級別】：碩士
【學位授予年份】：2015
【分類號】：R655.3

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本文編號：1955070