過氧化物酶增殖體激活受體β對(duì)急性肺損傷大鼠肺組織細(xì)胞凋亡的作用機(jī)制及影響
發(fā)布時(shí)間:2018-04-27 08:44
本文選題:急性肺損傷 + 過氧化物酶增殖體激活受體; 參考:《大連醫(yī)科大學(xué)》2013年碩士論文
【摘要】:目的探討過氧化物酶增殖體激活受體β(PPAR β)在急性肺損傷(ALI)發(fā)生發(fā)展中對(duì)肺組織細(xì)胞凋亡可能的作用,以期從新的視角揭示ALI/ARDS的發(fā)病機(jī)理,并為ALI/ARDS的防治提供新的理論基礎(chǔ)。 方法參照Cainazzo et al.方法復(fù)制失血性休克大鼠ALI模型,按完全隨機(jī)原則將12只SD大鼠分入兩組,失血性休克致急性肺損傷模型組(A組)和GW0742組(B組),每組6只老鼠。在造模后2小時(shí)采動(dòng)脈血,測(cè)定動(dòng)脈血氧分壓(PaO2)。放血猝死后,,取一塊左肺甲醛固定后制備切片,行病理形態(tài)學(xué)檢查;余左肺稱濕重后行支氣管肺泡灌洗,收集支氣管肺泡灌洗液(BALF)及右肺部分組織單細(xì)胞懸液,采用Annexin-V/PI雙染方法進(jìn)行細(xì)胞凋亡率檢測(cè);灌洗后左肺置于烘箱內(nèi)80℃干烤24h后稱干重,并計(jì)算肺組織濕/干重(W/D)值。 結(jié)果B組的PaO2均較A組顯著升高(P0.05)。B組的W/D比值、病理學(xué)積分、BALF細(xì)胞及肺組織細(xì)胞凋亡率均較A組顯著降低(P0.05)。 結(jié)論GW0742是PPAR β的激動(dòng)劑,通過抑制細(xì)胞凋亡對(duì)ALI肺組織起到一定程度的保護(hù)作用,減輕ALI肺組織的炎癥,改善PaO2。PPAR β在ALI發(fā)生、發(fā)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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