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目的观察前列地尔对大鼠肾缺血再灌注损伤的保护作用。方法首先建立大鼠肾缺血再灌注损伤动物模型,并将实验大鼠随机分为3组,即正常对照组(Control)、肾缺血再灌注损伤组(I/R)和前列地尔治疗组(前列地尔+I/R)。实验结束后检测大鼠血浆及肾组织中脂质过氧化代谢产物丙二醛(MDA)和超氧化物歧化酶(SOD)的活性,并观察大鼠肾脏组织结构的变化。结果大鼠发生肾脏缺血再灌注损伤时,血浆和肾组织中脂质过氧化代谢产物MDA的含量明显升高(P<0.05),而SOD的活性则明显降低(P<0.05)。在大鼠肾脏缺血再灌注损伤前预先给予前列地尔,能够明显抑制上述指标的变化,同时可以减轻大鼠肾脏组织超微结构的损伤。结论前列地尔可以降低大鼠血浆和肾组织中MDA的含量,升高SOD的水平,对大鼠肾缺血再灌注损伤具有明显的保护作用。
Objective To observe the protective effect of alprostadil on renal ischemia-reperfusion injury in rats. Methods The rat model of renal ischemia-reperfusion injury was established. The experimental rats were randomly divided into three groups: control group, I / R group and alprostadil treatment Group (alprostadil + I / R). After the experiment, the activity of lipid peroxidation metabolites malondialdehyde (MDA) and superoxide dismutase (SOD) in rat plasma and kidney tissue were detected, and the change of rat kidney tissue structure was observed. Results The renal MDA content in plasma and kidney increased significantly (P <0.05) and the activity of SOD decreased significantly (P <0.05) in rats with renal ischemia / reperfusion injury. Prolonged administration of alprostadil before ischemia-reperfusion injury in rat kidneys could significantly inhibit the changes of these indexes and at the same time reduce the ultrastructural damage of rat kidney tissue. Conclusion Alprostadil can reduce the content of MDA and increase the level of SOD in the plasma and kidney of rats, and has a significant protective effect on renal ischemia-reperfusion injury in rats.