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本实验旨在探讨金属硫蛋白是否参与肺缺血预处理(ischemic preconditioning,IP)的保护作用。实验用健康雄性Sprague-Dawley大鼠24只,随机分为对照组、肺缺血/再灌注(ischemia-reperfusion,I/R)组和IP组,对比观察各组肺组织中金属硫蛋白(metallothionein,MT)的含量,血清中丙二醛(malondialdehyde,MDA)含量、超氧化物歧化酶(superoxide dismutase,SOD)及髓过氧化物酶(myeloperoxidase,MPO)活性的变化,用原位缺口末端标记法(TUNEL)检测肺组织细胞的凋亡情况,用透射电镜观察肺组织超微结构的改变。结果显示,与对照组相比,I/R组肺组织中MT的含量显著下降(P<0.05),血清MDA含量、MPO活性明显升高(P<0.01),SOD活性明显下降(P<0.01),凋亡指数(apoptosis index,AI)显著增高(P<0.01),肺组织超微结构发生异常改变;与I/R组相比,IP组肺组织中MT的含量显著升高(P<0.01),血清MDA含量、MPO活性明显下降,SOD活性明显升高(P<0.05或P<0.01),AI为14.76±1.35,显著低于I/R组(P<0.01),肺组织超微结构显著改善。根据以上结果,我们推断诱导MT的产生可能是IP肺保护作用的机制之一。
This experiment aimed to investigate whether metallothionein is involved in the protective effect of ischemic preconditioning (IP). Twenty-four healthy male Sprague-Dawley rats were randomly divided into control group, ischemia-reperfusion (I / R) group and IP group. The levels of metallothionein , MT), serum malondialdehyde (MDA) content, superoxide dismutase (SOD) and myeloperoxidase (MPO) activity were detected by in situ nick end labeling TUNEL assay was used to detect the apoptosis of lung tissue cells. The ultrastructural changes of lung tissue were observed by transmission electron microscope. The results showed that compared with the control group, the content of MT in lung tissue of I / R group decreased significantly (P <0.05), the content of MDA in serum and MPO activity increased (P <0.01) and the activity of SOD decreased significantly (P <0.01 ), The apoptosis index (AI) increased significantly (P <0.01) and the ultrastructure of lung tissue changed abnormally. Compared with I / R group, the content of MT in lung tissue of IP group increased significantly (P < 0.01). The content of MDA and the activity of MPO in serum were significantly decreased, the activity of SOD was significantly increased (P <0.05 or P <0.01), AI was 14.76 ± 1.35, significantly lower than that in I / R group (P <0.01) The structure is significantly improved. Based on the above results, we infer that induction of MT production may be one of the mechanisms of IP lung protection.