摘要
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 changes and relationships between the serum endogenously produced interleukin- 10 (IL - 10), nitric oxide synthase (NOS) and inducible nitric oxide synthase (iNOS) in acute myocardial ischemia and reperfusion. Methods Forty -two rats were randomly divided into two groups: myocardial ischemia and reperfusion group (the control group) and methylprednisolone treatment group. The rats in the control group and methylprednisolone treatment group received intravenous injection of placebo and meth- ylprednisolone before ischemia respectively. The plasma IL - 10, NOS and iNOS were detected at 0. 5 h after ischaemia and 0. 5h , 2 h after reperfusion, respectively. Result The plasma IL - 10, NOS and iNOS gradually increased at 0. 5 h after ischaemia and 0. 5h , 2 h after reperfusion in the two groups. The levels of plasma IL - 10 were significantly higher in the methylprednisolone treatment group in different time points than those in the control ( all P 〈 0. 05). The levels of plasma NOS and iNOS were significantly lower in the methylprednisolone treatment group in different time points than those in the control ( all P 〈 0.05). The level of IL - 10 was negatively associated with the level of NOS and iNOS respectively ( NOS : r = - 0. 830, P 〈 0. 01 ; iNOS : r = - 0. 788, P 〈 0. 01 ). Conclusion Methylprednisolone facilitates the expression of endogenous IL - 10 during myocardial ischemia and reperfusion in rats. The endogenous IL - 10 plays a protective role on the myocardial ischemia and reperfusion through the suppression of NOS and iNOS which involves in the suppression of inflammatory reaction and the reduction of ischemical reperfusion injury.
出处
《中国医师杂志》
CAS
2005年第12期1619-1621,共3页
Journal of Chinese Physician