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目的 观察丝裂原活化蛋白激酶 (MAPKs)在外源性一氧化碳 (CO)抗大鼠肢体缺血再灌注 (IR)所致肺损伤中的作用。方法 健康SD大鼠 ,随机分为 4组 (每组n =8) :对照组 (Con trol)、Control +CO、IR和IR +CO组。复制大鼠双后肢缺血及再灌注后肺损伤模型。IR +CO和Control +CO组在再灌注前 1h或相应时间点置含CO的空气中 ,其余两组呼吸空气。观察大鼠肺组织学、肺组织中中性粒细胞 (PMN )数目、肺组织湿重和干重之比 (W /D)、丙二醛 (MDA)含量以及动物生存情况变化。应用Westernblotting检测肺组织中三种磷化MAPKs ,即细胞外信号调节激酶(ERK)、c Jun氨基末端激酶 (JNK)和 p3 8表达的变化。 结果 与Contorl组相比 ,IR组动物死亡率、肺组织PMN数目、W /D、MDA含量以及磷酸化ERK、JNK和p3 8表达均显著增高 ;与IR组相比 ,IR +CO组IR组动物死亡率、肺组织中PMN数目、W /D和MDA含量均显著降低、肺损伤减轻 ,p3 8表达显著增高 ,JNK表达显著降低 ,ERK表达无显著变化。结论 MAPKs信号通路参与了外源性CO抗大鼠肢体IR所致肺损伤作用的分子机制。
Objective To investigate the role of mitogen-activated protein kinases (MAPKs) in exogenous carbon monoxide (CO) -induced lung injury induced by limb ischemia-reperfusion (IR) in rats. Methods Healthy SD rats were randomly divided into 4 groups (n = 8 in each group): Control group, Control + CO, IR and IR + CO groups. Rat models of lung injury after double - hind limb ischemia and reperfusion in rats. In the IR + CO and Control + CO groups, CO-containing air was applied at 1 hour before reperfusion or at the corresponding time points, and the remaining two groups of breathing air. The lung histology, the number of neutrophils (PMNs), the ratio of W / D (wet / dry weight), the content of malondialdehyde (MDA) and the survival of animals were observed. Western blotting was used to detect the expression of three phosphorylated MAPKs in lung tissue, namely, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) Results Compared with the Contorl group, the mortality, the number of PMN, the W / D, the MDA content and the expressions of phosphorylated ERK, JNK and p38 in the IR group were significantly increased. Compared with the IR group, IR + CO IR group Animal mortality, PMN number, W / D and MDA content in lung tissue were significantly decreased, lung injury was alleviated, p3 8 expression was significantly increased, JNK expression was significantly reduced, ERK expression was not significantly changed. Conclusion MAPKs signaling pathway is involved in the molecular mechanism of exogenous CO on lung injury induced by IR in rats.