过氧化物酶增殖体激活受体β对急性肺损伤大鼠肺组织细胞凋亡的作用机制及影响

发布时间：2018-04-27 08:44

  本文选题：急性肺损伤 + 过氧化物酶增殖体激活受体　； 参考：《大连医科大学》2013年硕士论文

【摘要】：目的探讨过氧化物酶增殖体激活受体β（PPAR β）在急性肺损伤（ALI）发生发展中对肺组织细胞凋亡可能的作用,以期从新的视角揭示ALI/ARDS的发病机理,并为ALI/ARDS的防治提供新的理论基础。 方法参照Cainazzo et al.方法复制失血性休克大鼠ALI模型，按完全随机原则将12只SD大鼠分入两组，失血性休克致急性肺损伤模型组（A组）和GW0742组（B组），每组6只老鼠。在造模后2小时采动脉血，测定动脉血氧分压（PaO2）。放血猝死后，，取一块左肺甲醛固定后制备切片，行病理形态学检查；余左肺称湿重后行支气管肺泡灌洗，收集支气管肺泡灌洗液（BALF）及右肺部分组织单细胞悬液，采用Annexin-V/PI双染方法进行细胞凋亡率检测；灌洗后左肺置于烘箱内80℃干烤24h后称干重，并计算肺组织湿/干重（W/D）值。 结果B组的PaO2均较A组显著升高（P0.05）。B组的W/D比值、病理学积分、BALF细胞及肺组织细胞凋亡率均较A组显著降低（P0.05）。 结论GW0742是PPAR β的激动剂，通过抑制细胞凋亡对ALI肺组织起到一定程度的保护作用，减轻ALI肺组织的炎症，改善PaO2。PPAR β在ALI发生、发展中起重要作用。
[Abstract]:Objective to investigate the possible role of peroxidase proliferator activated receptor 尾 (PPAR 尾) in the development of acute lung injury (Ali) in lung tissue apoptosis, in order to reveal the pathogenesis of ALI/ARDS from a new perspective and provide a new theoretical basis for the prevention and treatment of ALI/ARDS. Methods Cainazzo et al. Methods the ALI model of hemorrhagic shock rats was established and 12 SD rats were randomly divided into two groups: group A (group A) and group B (GW0742 group: 6 rats in each group). The arterial blood was collected 2 hours after modeling, and the partial pressure of oxygen in arterial blood was measured. After sudden bleeding death, a piece of left lung was fixed with formaldehyde to prepare the sections, and the remaining left lung was given bronchoalveolar lavage after weighing wet, and the BALF) and the single cell suspension of the right lung tissue were collected. The rate of apoptosis was detected by Annexin-V/PI double staining method, the left lung was dried at 80 鈩

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