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目的探讨缺血再灌注中白介素10(IL-10)、总一氧化氮合酶(NOS)及诱导型一氧化氮合酶(iNOS)变化及关系,为临床诊治缺血再灌注损伤提供实验依据。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(药物组)2组,在心肌缺血前用甲基强的松龙(30mg/kg)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、NOS、iNOS。结果对照组与药物组自缺血0.5h、再灌注0.5h至2h IL-10、NOS、iNOS呈逐渐升高趋势,具有显著性差异(P<0.01),各时段内,药物组较对照组IL-10明显升高,差异有统计学意义(P<0.01~0.05);再灌注后药物组NOS,iNOS较对照组降低,差异有统计学意义(P<0.01~0.05)。IL-10分别与NOS、iNOS呈显著负相关(NOS:r=-0.830,P<0.01;iNOS:r=-0.788,P<0.01)。结论在大鼠心肌缺血再灌注中,甲基强的松龙可促进内源性IL-10大量释放;IL-10通过抑制NOS、iNOS的产生抑制炎症反应,减少心肌缺血再灌注损伤,发挥保护作用。
Objective To investigate the relationship between interleukin 10 (IL-10), total nitric oxide synthase (NOS) and inducible nitric oxide synthase (iNOS) during ischemia-reperfusion and to provide experimental evidence for clinical diagnosis and treatment of ischemia-reperfusion injury . Methods The rats were randomly divided into two groups: ischemia / reperfusion (control group) and methylprednisolone treatment group (drug group). The rats were pretreated with methylprednisolone (30mg / kg) The rats were pretreated with IL-10, NOS and iNOS for 0.5h and 0.5h after reperfusion for 2 hours. Results The levels of IL-10, NOS and iNOS in control group and drug group increased gradually from 0.5h to 0.5h to 2h after reperfusion, with significant difference (P <0.01). In each time period, compared with control group (P <0.01 ~ 0.05). After reperfusion, the levels of NOS and iNOS in the drug group were significantly lower than those in the control group (P <0.01 ~ 0.05). IL-10 and NOS, iNOS were significantly negatively correlated (NOS: r = -0.830, P <0.01; iNOS: r = -0.788, P <0.01). Conclusion Methylprednisolone can promote the release of endogenous IL-10 in myocardial ischemia reperfusion in rats. IL-10 can inhibit the inflammatory reaction and reduce the myocardial ischemia-reperfusion injury by inhibiting the production of NOS and iNOS, Play a protective role.