中介素1-53对肺缺血再灌注损伤大鼠肺组织PPAR-γ的影响

发布时间：2018-07-02 20:04

本文选题：肺缺血再灌注损伤 + 中介素1-53　；参考：《山西医科大学》2010年硕士论文

【摘要】： 目的：观察中介素1-53对肺缺血再灌注损伤(LIRI)大鼠中过氧化物酶增殖物激活受体γ(PPAR-γ)的影响方法：建立大鼠在体肺缺血再灌注模型。将72只健康雄性Wistar大鼠随机分为3组：手术对照组(C组),缺血再灌注组(IR组),中介素1-53干预组(D组)。每组分别于夹闭缺血的第45min、再灌注60、120min3个时点处死8只大鼠,并取血浆和右肺中叶组织,观察肺组织病理形态变化,测定肺组织湿干质量比值(W/D)、髓过氧化物酶(MPO)活性、肺组织匀浆CINC-1蛋白含量,免疫组织化学技术检测肺组织PPAR-Y蛋白的变化,半定量RT-PCR方法检测肺组织中PPAR-Y的改变。结果：1.成功建立在体大鼠肺缺血再灌注模型。2.①肺组织病理变化：IR组于缺血再灌注后肺组织损伤进行性加重,肺泡间隔炎性细胞浸润、毛细血管充血、肺泡腔内炎性细胞及炎性液体渗出渐显著,而D组,肺组织充血、水肿、炎性细胞浸润均较IR组减轻；②肺组织W/D比值：缺血45min时,各组W/D值无明显变化,再灌注后,IR、D组肺组织W/D均升高,其中以IR组升高明显,D组虽高于C组,但较IR组明显降低(P0.05)；③肺组织MPO活性：IR组和D组随再灌注时间的延长MPO活性逐渐升高,且较C组升高(P0.05)；但D组肺组织MPO活性要低于IR组(P0.05)；④肺组织CINC-1含量变化：与手术对照组比较,IR组各时相点CINC-1含量明显增加(P0.05),经IMD1-53干预后CINC-1含量明显下降(P0.05)；⑤肺组织PPAR-Y mRNA和蛋白的变化：在各个时点,IR组PPAR-Y mRNA表达均较C组下降(P0.05),但D组表达水平较IR组升高,(P0.05)但仍低于C组；肺组织PPAR-Y蛋白表达变化情况与PPAR-Y mRNA变化基本一致,只是蛋白表达迟于转录水平两个小时。结论：中介素1-53对于大鼠肺脏缺血再灌注损伤具有一定的保护作用,可能与其上调PPAR-Y表达、激活PPAR-Y,从而抑制CINC-1蛋白表达,降低肺组织MPO活性等发挥抗炎作用有关。
[Abstract]:Aim: to observe the effect of mediator 1-53 on peroxidase proliferator activated receptor 纬 (PPAR- 纬) 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.
【学位授予单位】：山西医科大学
【学位级别】：硕士
【学位授予年份】：2010
【分类号】：R363

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