本文選題：高濃度氧 + 肺損傷��； 參考：《瀘州醫(yī)學(xué)院》2013年碩士論文

【摘要】：目的研究?jī)?nèi)質(zhì)網(wǎng)應(yīng)激在高氧誘導(dǎo)早產(chǎn)鼠肺損傷中的作用。 方法將新生早產(chǎn)Wistar鼠48只在生后12小時(shí)隨機(jī)分為對(duì)照組、高氧組，其體質(zhì)量無統(tǒng)計(jì)學(xué)意義，對(duì)照組置于21%氧濃度空氣中，高氧組則吸入95%的高分子體積氧建立高氧肺損傷模型，兩者其他條件相同。兩組小鼠在上述相應(yīng)處理后1d、3d、7d分批以斷頸放血的方式處死，每組取動(dòng)物8只，然后取肺組織。以左肺制作石蠟切片，采用蘇木精一伊紅（HE）染色觀察肺組織病理改變；免疫組織化學(xué)鏈霉菌抗生物素蛋白-過氧化物酶連結(jié)(streptavidin-peroxidase,SP）法檢測(cè)內(nèi)質(zhì)網(wǎng)應(yīng)激相關(guān)指標(biāo)：ERp57; c/EBP同源蛋白（CHOP）在各組肺組織內(nèi)的表達(dá)；采用原位末端標(biāo)記法（TUNEL）檢測(cè)肺細(xì)胞凋亡情況。 結(jié)果(1)肺組織病理學(xué)改變：光鏡下觀察對(duì)照組大鼠肺組織結(jié)構(gòu)正常。高氧組暴露1d肺組織病理學(xué)檢查無明顯差異，均為大而不規(guī)則的肺泡腔。高氧組暴露3d，可見小血管擴(kuò)張，肺泡上皮腫脹，肺泡腔及間質(zhì)內(nèi)有大量紅細(xì)胞和炎細(xì)胞滲出；暴露7d上述變化更明顯，(2) ERp57; c/EBP同源蛋白（CHOP）在肺組織的表達(dá)與分布：ERp57在肺組織中普遍表達(dá)于肺泡上皮細(xì)胞、血管內(nèi)皮細(xì)胞、支氣管上皮細(xì)胞的細(xì)胞質(zhì)中。對(duì)照組ERp57表達(dá)很少，高氧組ERp57隨著高氧暴露時(shí)間的延長(zhǎng)表達(dá)逐漸增多，與對(duì)照組相比有統(tǒng)計(jì)學(xué)差異。（平均光密度值A(chǔ)OD:對(duì)照組1d0.235±0.023、3d0.257±0.056、7d0.267±0.058；高氧組1d0.320±0.02、3d0.347±0.054、7d0.400±0.0273d、7d P＜0.05）; c/EBP同源蛋白（CHOP）在肺組織中也普遍表達(dá)于肺泡上皮細(xì)胞、血管內(nèi)皮細(xì)胞、支氣管上皮細(xì)胞的細(xì)胞質(zhì)中。對(duì)照組c/EBP同源蛋白（CHOP）表達(dá)微弱，高氧組c/EBP同源蛋白（CHOP）隨著暴露時(shí)間的延長(zhǎng)表達(dá)逐漸明顯，與對(duì)照組相比有統(tǒng)計(jì)學(xué)差異。（平均光密度值A(chǔ)OD:對(duì)照組1d0.165±0.037、3d0.268±0.036、7d0.207±0.034；高氧組1d0.307±0.048、3d0.318±0.06、7d0.330±0.0541d、3d、7d P＜0.05）；(3) TUNEL檢測(cè)凋亡細(xì)胞：對(duì)照組也可見少許TUNEL陽(yáng)性細(xì)胞，高氧組則隨著高氧暴露時(shí)間的延長(zhǎng)TUNEL陽(yáng)性細(xì)胞明顯增多，與對(duì)照組相比有明顯統(tǒng)計(jì)學(xué)差異。(凋亡指數(shù)Apoptotic index, AI：對(duì)照組1d14.44±1.10、3d14.60±2.06、7d14.35±1.45；高氧組1d25.49±1.25、3d44.97±1.82、7d55.34±1.761d、3d、7d P＜0.01);(4) ERp57、c/EBP同源蛋白表達(dá)與細(xì)胞凋亡指數(shù)相關(guān)性：采用直線相關(guān)分析結(jié)果如下：細(xì)胞凋亡指數(shù)和ERP57AOD比較，r=0.789，P0.01；與c/EBP同源蛋白比較r=0.645，P0.01,均提示呈顯著正相關(guān)。 結(jié)論1.高氧暴露可導(dǎo)致早產(chǎn)鼠肺組織產(chǎn)生急性肺損傷病理性改變。而這一表現(xiàn)隨著高氧暴露時(shí)間延長(zhǎng)顯示更明顯。 2.高氧暴露可致新生大鼠肺組織ERp57; c/EBP同源蛋白表達(dá)增加,提示內(nèi)質(zhì)網(wǎng)應(yīng)激細(xì)胞凋亡參與了高氧肺損傷，并發(fā)揮重要作用，具體機(jī)制仍需要進(jìn)一步研究。 3. ERp57; c/EBP同源蛋白表達(dá)與細(xì)胞凋亡指數(shù)動(dòng)態(tài)變化具有相關(guān)性。
[Abstract]:Objective to study the role of endoplasmic reticulum stress in hyperoxia-induced lung injury in preterm rats. Methods 48 preterm Wistar rats were randomly divided into control group (n = 48) and hyperoxia group (n = 48). The control group was placed in air with 21% oxygen concentration and the hyperoxia group inhaled 95% high molecular weight oxygen to establish hyperoxia-induced lung injury model. The other two conditions are the same. The mice of the two groups were killed in batches at 1 day, 3 days and 7 days after the corresponding treatment, and 8 animals were taken from each group, and then lung tissue was taken out. Paraffin sections were made from the left lung, and the pathological changes of lung tissue were observed by hematoxylin-eosin (HEH) staining. Immunohistochemical streptavidin-peroxidase (SPP) method was used to detect the expression of c/EBP homologue protein (CHOP) and endoplasmic reticulum stress (ERp57) in lung tissues, and Tunel was used to detect the apoptosis of lung cells. Results 1) pathological changes of lung tissue: the lung tissue structure of the control group was normal under light microscope. There was no significant difference in histopathological examination of lung in hyperoxia group after 1 day exposure, all of them were large and irregular alveolar lumen. In hyperoxia group, small vessels dilated, alveolar epithelium swelling, erythrocytes and inflammatory cells exudated in alveolar cavity and interstitium. The expression and distribution of c/EBP homologue protein (CHOP5) in lung tissues were found in alveolar epithelial cells, vascular endothelial cells and bronchial epithelial cells, and the expression and distribution of c/EBP homologous protein CHOP57 in lung tissue were also found in the cytoplasm of alveolar epithelial cells, vascular endothelial cells and bronchial epithelial cells. The expression of ERp57 in hyperoxia group increased with the prolongation of hyperoxia exposure time, and there was statistical difference between hyperoxia group and control group. (average optical density value: 1d0.235 鹵0.023 鹵0.056 days 0.257 鹵0.056 days 0.267 鹵0.058; 1d0.320 鹵0.02 鹵0.054 d 0.347 鹵0.054 d 0.347 鹵0.027 3 d 7d P < 0.05; c/EBP homologous protein Chopp also expressed in alveolar epithelial cells, vascular endothelial cells, bronchial epithelial cells) in lung tissue. The expression of c/EBP homologue protein in control group was weak, and the expression of c/EBP homologue protein in hyperoxia group was gradually obvious with the prolongation of exposure time, and there was significant difference between the control group and the control group. (mean optical density: 1d0.165 鹵0.037 鹵0.036 鹵0.268 鹵0.036 鹵0.207 鹵0.034 on day 0.207 鹵0.034; 1d0.307 鹵0.048 鹵0.06 鹵0.318 鹵0.06 on 7d 0.330 鹵0.0541d / 3 d / d P < 0.05D / d P < 0.05D / d) apoptotic cells were detected by TUNEL. A few TUNEL positive cells were also found in the control group, while in the hyperoxia group, the number of TUNEL positive cells increased significantly with the prolongation of the hyperoxia exposure time (P < 0.05), and the number of TUNEL positive cells in the hyperoxia group was significantly higher than that in the hyperoxia group (P < 0.05). Compared with the control group, there was significant statistical difference. (Apoptotic index, AI: control 1d14.44 鹵1.10d14.60 鹵2.06d14.35 鹵1.45d; hyperoxia group 1d25.49 鹵1.252d44.97 鹵1.82d54.97 鹵1.82d7d 55.34 鹵1.761dcEBP protein expression and apoptosis index P < 0.01p57cP / EBP homologous protein expression and apoptosis index: the results of linear correlation analysis were as follows: apoptotic index and ERP57AOD were 0.789P0.01; compared with c/EBP homologous protein ru 0.645P0.01; P < 0.01; P < 0.01); the expression of ERp57cEBP homologous protein was compared with c/EBP homologue protein. The results of linear correlation analysis were as follows: the apoptosis index and ERP57AOD were 0.789P0.01and 0.645P0.01respectively. There was a significant positive correlation. Conclusion 1. Hyperoxia exposure may lead to pathological changes of acute lung injury in preterm rats. This performance was more obvious with the time of hyperoxia exposure. 2. The expression of ERp57; c/EBP homologous protein in lung tissue of neonatal rats was increased after hyperoxia exposure, suggesting that endoplasmic reticulum stress cells apoptosis was involved in hyperoxia lung injury and played an important role. The specific mechanism still needs to be further studied. 3. ERp57; c/EBP homologous protein expression was correlated with the dynamic change of apoptosis index.
【學(xué)位授予單位】：瀘州醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2013
【分類號(hào)】：R722.6

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