盛西陵 王东明 陈畅.大鼠心肌缺血再灌注IL-10的变化及强的松龙干预[J].实用中西医结合临床,2004,(5):5-6 |
大鼠心肌缺血再灌注IL-10的变化及强的松龙干预 |
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DOI: |
中文关键词: 缺血再灌注损伤 甲基强的松龙 白介素10 磷酸肌酸激酶同功酶 实验研究 |
英文关键词: ischemia/reperfusion Interleukin-10 methylprednisolone |
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中文摘要: |
目的:探讨缺血再灌注中白介素10(IL-10)的变化及甲基强的松龙对其影响,为临床缺血再灌注损伤的诊治提供实验依据。方法:将大鼠随机分成缺血再灌注(对照组)、甲基强的松龙治疗组2组,每组内再随机分成缺血0.5h、再灌注0.5h及再灌注2h3个亚组。在心肌缺血前用甲基强的松龙对药物组大鼠预处理。分别测定缺血0.5h、再灌注0.5h及2h血清IL-10、CK-MB的水平。结果:(1)对照组与药物组自缺血0.5h、再灌注0.5h至2h IL-10呈逐渐升高趋势,具有显著性差异,两两比较具统计学意义(P <0.05);各时段内,药物组较对照组明显升高,具有显著性差异 (再灌注 0.5 h P <0.05; 再灌注2h P <0.01)。(2)对照组与药物组CK-MB在缺血0.5h出现升高,再灌注2h明显升高,具有显著性差异(对照组:T =14.609,P <0.01;药物组:T =55.707,P <0.05),两两比较具统计学意义(P <0.05);相同时段内,与对照组相比较,药物组CK-MB升高延迟,在心肌缺血0.5h略有降低,但无统计学意义(P >0.05);在再灌注2h降低, 呈显著性差异(P <0.05)。结论:甲基强的松龙可促进内源性IL-10大量释放,减少心肌缺血再灌注损伤,发挥保护作用。 |
英文摘要: |
Objective: Investigated the change of serum interleukin-10(IL-10) and effecting of methylprednisolone in acute myocardial ischemia and reperfusion. Methods: put equally 42 rats into two groups, 21 control rats who received i.v. bolus placebo and 21 administration rats who received i.v. bolus methylprednisolone before ischemia, Plasma IL-10 by ELISA was measured at 0.5 hour after ischaemia and 0.5, 2 hours after reperfusion, meantime serum creatine kinase isoenzyme MB(CK-MB) were measured at respective time points.Result: Significant levels of IL-10 were produced in both control and administration groups from ischemia 0.5 hour to 0.5 hour, 2 hours after myocardial reperfusion. IL-10 level in administration group was remarkably higher than that in control group at the same time point after reperfusion. Meantime serum CK-MB concentrations were increased gradually from 0.5 hours after ischemia to 2 hours after reperfusion and increased significantly at 2 hours after reperfusion (P <0.05). CK-MB concentrations in administration group were statistically lower than those of control group after reperfusion while the increase of CK-MB was delayed. Conclusion: Methylprednisolone enhance highly release of IL-10.and serves to protect the ischemia and reperfued myocardia |
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