后處理對(duì)缺血再灌注損傷鼠肺EGR-1表達(dá)的影響
發(fā)布時(shí)間：2018-11-06 11:16
【摘要】：目的：研究后處理對(duì)在體缺血再灌注損傷大鼠肺EGR-1表達(dá)的影響,并分析其可能的肺保護(hù)作用機(jī)制。 方法：建立大鼠在體肺臟缺血再灌注損傷模型,將24只SD大鼠隨機(jī)分為假手術(shù)(Sham)組、缺血再灌注(I/R)組和缺血后處理(IPostC)組,每組8只。在體大鼠I/R損傷模型制備完成后,阻斷左肺門,終止血供及通氣,造成左肺缺血,達(dá)預(yù)定時(shí)間后松開(kāi)阻斷帶恢復(fù)血供及通氣形成再灌注。Sham組只游離左側(cè)肺門、套阻斷帶但不阻斷,等待3h后直接取標(biāo)本；I/R組缺血1h后再灌注2h; IPostC組缺血1h后給予重復(fù)三次的5min灌注和5min缺血的后處理,繼以恢復(fù)血供及通氣再灌注1.5h。3組實(shí)驗(yàn)結(jié)束后均留取左側(cè)肺組織：取部分制成10%的組織勻漿,用于測(cè)定髓過(guò)氧化物酶(MPO)的含量；留取小塊肺組織測(cè)定肺濕/干重比(W/D),并在光鏡下觀察肺組織的病理變化；RT-PCR法檢測(cè)其余左肺組織中EGR-1 mRNA及IL-1βmRNA的表達(dá)量。 結(jié)果：三組間各項(xiàng)檢測(cè)指標(biāo)比較,差異均有顯著性(P0.05)。①W/D值：與Sham組(4.4935±0.4171)比較,I/R組(6.6513±0.3820)明顯升高(P0.05)；而IPostC組(5.5151±0.2693)則明顯低于I/R組(P0.05)。②肺組織中MPO的含量：與Sham組(1.1847±0.2636)比較,I/R組(2.2732±0.5593)明顯升高(P0.05)；而與I/R組相比,IPostC組(1.6317±0.2015)明顯降低(P0.05)。③肺組織IL-1βmRNA的表達(dá)量：與Sham組(0.2308±0.0083)比較,I/R組(0.5500±0.0281)明顯升高(P0.05)；而與I/R組比較,IPostC組(0.3661±0.0080)明顯降低(P0.05)。④肺組織EGR-1 mRNA的表達(dá)量：與Sham組(0.2975±0.0289)比較,I/R組(0.6147±0.0152)明顯升高(P0.05)；而與I/R組相比,IPostC組(0.4680±0.0166)明顯降低(P0.05)。⑤病理形態(tài)學(xué)觀察：Sham組肺間質(zhì)及肺泡基本完整,未見(jiàn)炎癥細(xì)胞浸潤(rùn)；I/R組均出現(xiàn)不同程度的肺泡水腫,毛細(xì)血管破裂出血,肺間質(zhì)增寬并有水腫,炎癥細(xì)胞浸潤(rùn),肺泡內(nèi)有較多血液成分滲出；IPostC組肺間質(zhì)輕度水腫,少量炎癥細(xì)胞浸潤(rùn),肺泡內(nèi)有少量血液成分滲出。 結(jié)論：后處理能夠明顯減輕鼠肺缺血再灌注損傷,從而起到肺保護(hù)作用。其機(jī)制可能與其抑制缺血再灌注損傷鼠肺組織中EGR-1及IL-1β的表達(dá)從而減輕肺組織炎癥反應(yīng)有關(guān)。
[Abstract]:Aim: to study the effect of post-treatment on the expression of EGR-1 in the lung of rats with ischemia-reperfusion injury in vivo and to analyze its possible protective mechanism. Methods: 24 SD rats were randomly divided into sham-operated (Sham) group, ischemia-reperfusion (I / R) group and post-ischemic (IPostC) group (8 rats in each group). After the model of I / R injury was made in rats, the left hilus was blocked, blood supply and ventilation were terminated, left lung ischemia was caused, and the blood supply was restored and ventilated reperfusion was formed after the release of the blocking band. The Sham group only left the left pulmonary hilum. The specimens were collected directly after 3 hours. In I / R group, 1 h after ischemia and 2 h after reperfusion; After 1 hour of ischemia, IPostC group was treated with repeated 5min perfusion and 5min ischemia, then the left lung tissue was retained after blood supply recovery and ventilation reperfusion in 1.5h.3 group: 10% tissue homogenate was obtained. To determine the content of myeloperoxidase (MPO); Lung wet / dry weight ratio (W / D) was measured in small lung tissue and the pathological changes of lung tissue were observed under light microscope. The expression of EGR-1 mRNA and IL-1 尾 mRNA in other left lung tissues were detected by RT-PCR method. Results: there were significant differences among the three groups (P0.05). 1W/D value: compared with Sham group (4.4935 鹵0.4171), I / R group (6.6513 鹵0.3820) significantly increased (P0.05); The content of MPO in lung tissue in IPostC group (5.5151 鹵0.2693) was significantly lower than that in I / R group (P0.05). Compared with Sham group (1.1847 鹵0.2636), I / R group (2.2732 鹵0.5593) was significantly higher (P0.05). Compared with I / R group, IPostC group (1.6317 鹵0.2015) significantly decreased the expression of IL-1 尾 mRNA in lung tissue: compared with Sham group (0.2308 鹵0.0083), I / R group (0.5500 鹵0.0281) significantly increased the expression of IL-1 尾 mRNA (P0.05). Compared with I / R group, IPostC group (0.3661 鹵0.0080) significantly decreased the expression of EGR-1 mRNA in lung tissue (P0.05). Compared with Sham group (0.2975 鹵0.0289), I / R group (0.6147 鹵0.0152) significantly increased the expression of EGR-1 mRNA (P0.05). Compared with I / R group, IPostC group (0.4680 鹵0.0166) was significantly lower than that of I / R group (P0.05). 5 Pathomorphological observation showed that interstitial and alveolar infiltration was almost intact in Sham group, and no inflammatory cell infiltration was found. In the I / R group, alveolar edema, capillary rupture and hemorrhage, pulmonary interstitial enlargement and edema, inflammatory cell infiltration and blood component exudation in the alveoli were found in all cases. In IPostC group, the interstitial edema was mild, a small amount of inflammatory cells infiltrated, and a few blood components exudated in the alveoli. Conclusion: post-treatment can significantly reduce lung ischemia-reperfusion injury and thus play a protective role in lung injury. The mechanism may be related to its inhibition of the expression of EGR-1 and IL-1 尾 in the lung tissue of rats with ischemia-reperfusion injury, thereby reducing the inflammatory response of the lung tissue.
【學(xué)位授予單位】：遵義醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2011
【分類號(hào)】：R363
本文編號(hào)：2314112
[Abstract]:Aim: to study the effect of post-treatment on the expression of EGR-1 in the lung of rats with ischemia-reperfusion injury in vivo and to analyze its possible protective mechanism. Methods: 24 SD rats were randomly divided into sham-operated (Sham) group, ischemia-reperfusion (I / R) group and post-ischemic (IPostC) group (8 rats in each group). After the model of I / R injury was made in rats, the left hilus was blocked, blood supply and ventilation were terminated, left lung ischemia was caused, and the blood supply was restored and ventilated reperfusion was formed after the release of the blocking band. The Sham group only left the left pulmonary hilum. The specimens were collected directly after 3 hours. In I / R group, 1 h after ischemia and 2 h after reperfusion; After 1 hour of ischemia, IPostC group was treated with repeated 5min perfusion and 5min ischemia, then the left lung tissue was retained after blood supply recovery and ventilation reperfusion in 1.5h.3 group: 10% tissue homogenate was obtained. To determine the content of myeloperoxidase (MPO); Lung wet / dry weight ratio (W / D) was measured in small lung tissue and the pathological changes of lung tissue were observed under light microscope. The expression of EGR-1 mRNA and IL-1 尾 mRNA in other left lung tissues were detected by RT-PCR method. Results: there were significant differences among the three groups (P0.05). 1W/D value: compared with Sham group (4.4935 鹵0.4171), I / R group (6.6513 鹵0.3820) significantly increased (P0.05); The content of MPO in lung tissue in IPostC group (5.5151 鹵0.2693) was significantly lower than that in I / R group (P0.05). Compared with Sham group (1.1847 鹵0.2636), I / R group (2.2732 鹵0.5593) was significantly higher (P0.05). Compared with I / R group, IPostC group (1.6317 鹵0.2015) significantly decreased the expression of IL-1 尾 mRNA in lung tissue: compared with Sham group (0.2308 鹵0.0083), I / R group (0.5500 鹵0.0281) significantly increased the expression of IL-1 尾 mRNA (P0.05). Compared with I / R group, IPostC group (0.3661 鹵0.0080) significantly decreased the expression of EGR-1 mRNA in lung tissue (P0.05). Compared with Sham group (0.2975 鹵0.0289), I / R group (0.6147 鹵0.0152) significantly increased the expression of EGR-1 mRNA (P0.05). Compared with I / R group, IPostC group (0.4680 鹵0.0166) was significantly lower than that of I / R group (P0.05). 5 Pathomorphological observation showed that interstitial and alveolar infiltration was almost intact in Sham group, and no inflammatory cell infiltration was found. In the I / R group, alveolar edema, capillary rupture and hemorrhage, pulmonary interstitial enlargement and edema, inflammatory cell infiltration and blood component exudation in the alveoli were found in all cases. In IPostC group, the interstitial edema was mild, a small amount of inflammatory cells infiltrated, and a few blood components exudated in the alveoli. Conclusion: post-treatment can significantly reduce lung ischemia-reperfusion injury and thus play a protective role in lung injury. The mechanism may be related to its inhibition of the expression of EGR-1 and IL-1 尾 in the lung tissue of rats with ischemia-reperfusion injury, thereby reducing the inflammatory response of the lung tissue.
【學(xué)位授予單位】：遵義醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2011
【分類號(hào)】：R363
【參考文獻(xiàn)】
相關(guān)期刊論文 前2條
1 梁貴友,牛義民,劉達(dá)興,徐剛,蔡慶勇;內(nèi)源性一氧化氮抗兔肺缺血再灌注損傷作用及其機(jī)制探討[J];四川大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2005年02期
2 鄒樹(shù);田伏洲;湯禮軍;黎冬暄;汪濤;石力;;早期生長(zhǎng)反應(yīng)基因-1與大鼠急性胰腺炎合并肺損傷[J];四川醫(yī)學(xué);2007年05期
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