本文選題：肺缺血再灌注損傷 + 中介素1-53�。� 參考：《山西醫(yī)科大學》2010年碩士論文

【摘要】： 目的：觀察中介素1-53對肺缺血再灌注損傷(LIRI)大鼠中過氧化物酶增殖物激活受體γ(PPAR-γ)的影響 方法：建立大鼠在體肺缺血再灌注模型。將72只健康雄性Wistar大鼠隨機分為3組：手術對照組(C組),缺血再灌注組(IR組),中介素1-53干預組(D組)。每組分別于夾閉缺血的第45min、再灌注60、120min3個時點處死8只大鼠,并取血漿和右肺中葉組織,觀察肺組織病理形態(tài)變化,測定肺組織濕干質量比值(W/D)、髓過氧化物酶(MPO)活性、肺組織勻漿CINC-1蛋白含量,免疫組織化學技術檢測肺組織PPAR-Y蛋白的變化,半定量RT-PCR方法檢測肺組織中PPAR-Y的改變。 結果：1.成功建立在體大鼠肺缺血再灌注模型。2.①肺組織病理變化：IR組于缺血再灌注后肺組織損傷進行性加重,肺泡間隔炎性細胞浸潤、毛細血管充血、肺泡腔內炎性細胞及炎性液體滲出漸顯著,而D組,肺組織充血、水腫、炎性細胞浸潤均較IR組減輕；②肺組織W/D比值：缺血45min時,各組W/D值無明顯變化,再灌注后,IR、D組肺組織W/D均升高,其中以IR組升高明顯,D組雖高于C組,但較IR組明顯降低(P0.05)；③肺組織MPO活性：IR組和D組隨再灌注時間的延長MPO活性逐漸升高,且較C組升高(P0.05)；但D組肺組織MPO活性要低于IR組(P0.05)；④肺組織CINC-1含量變化：與手術對照組比較,IR組各時相點CINC-1含量明顯增加(P0.05),經IMD1-53干預后CINC-1含量明顯下降(P0.05)；⑤肺組織PPAR-Y mRNA和蛋白的變化：在各個時點,IR組PPAR-Y mRNA表達均較C組下降(P0.05),但D組表達水平較IR組升高,(P0.05)但仍低于C組；肺組織PPAR-Y蛋白表達變化情況與PPAR-Y mRNA變化基本一致,只是蛋白表達遲于轉錄水平兩個小時。 結論：中介素1-53對于大鼠肺臟缺血再灌注損傷具有一定的保護作用,可能與其上調PPAR-Y表達、激活PPAR-Y,從而抑制CINC-1蛋白表達,降低肺組織MPO活性等發(fā)揮抗炎作用有關。
[Abstract]:Aim: to observe the effect of mediator 1-53 on peroxidase proliferator activated receptor 緯 (PPAR- 緯) in lung ischemia-reperfusion injury (LIRI) rats. Seventy-two healthy male Wistar rats were randomly divided into three groups: operation control group (group C), ischemia reperfusion group (IR group) and mediin-1-53 intervention group (group D). The rats in each group were killed at 45 min after ischemia. Plasma and middle lobe of right lung tissues were taken from each group. The changes of lung tissue were observed, and the wet / dry mass ratio (W / D) and the activity of myeloperoxidase (MPO) in lung tissue were measured. The contents of CINC-1 protein in lung homogenate, the changes of PPAR-Y protein in lung tissue by immunohistochemistry, and the changes of PPAR-Y protein in lung tissue were detected by semi-quantitative RT-PCR. The result is 1: 1. The pathological changes of lung tissue were successfully established in rats with lung ischemia reperfusion in vivo. The pathological changes of lung tissue in the 1: 1 IR group were progressive exacerbation of lung tissue injury, infiltration of inflammatory cells in alveolar septum and capillary congestion after ischemia / reperfusion. In group D, congestion, edema and infiltration of inflammatory cells in lung tissue decreased the ratio of W / D of lung tissue in group D: after ischemia of 45min, there was no significant change in the value of W / D in each group. After reperfusion, the lung tissue W- / D increased in IRD group. The MPO activity of lung tissue in IR group was significantly higher than that in C group, but significantly lower than that in IR group (P0.05). The MPO activity of lung tissue in group D and group D gradually increased with the prolongation of reperfusion time. Compared with the control group, the level of CINC-1 in lung tissue in group D was significantly higher than that in group C (P0.05), but the level of CINC-1 in group D was lower than that in group IR (P0.05). The content of CINC-1 in group D was significantly higher than that in group C (P0.05), and the content of CINC-1 in group D was significantly decreased after IMD1-53 intervention (P0.05). 5the changes of PPAR-Y mRNA and protein in lung tissue: PPAR-Y mRNA expression in IR group was lower than that in C group at all time points (P0.05), but the expression level of PPAR-Y mRNA in group D was higher than that in IR group (P0.05) but still lower than that in C group, the change of PPAR-Y protein expression in lung tissue was basically the same as that in PPAR-Y mRNA. Only the protein expression was two hours later than the transcription level. Conclusion: mediator 1-53 has a protective effect on lung ischemia-reperfusion injury in rats, which may be related to its anti-inflammatory effect by up-regulating the expression of PPAR-Y and activating PPAR-Y, thus inhibiting the expression of CINC-1 protein and reducing the activity of MPO in lung tissue.
【學位授予單位】：山西醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2010
【分類號】：R363

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