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目的:研究黄芪多糖在未成年大鼠心肌缺血再灌注炎性损伤中的作用。方法:1周龄雄性SD大鼠随机分为5组,假手术组(S组)、缺血再灌注组(I/R组)、黄芪多糖组(40 mg·kg~(-1),APS组、p38MAPK阻断剂SB203580组(5 mg·kg~(-1),SB组),APS+SB203580组(APS 40 mg·kg~(-1)+SB203580 5 mg·kg~(-1),APS+SB组),给药20 d后,进行冠状动脉左前降支结扎60 min后恢复血流再灌注120 min,经眼眶采血后处死大鼠。ELISA法和Western-blot法分别测定外周血和心肌组织中TNF-α、NF-κB、p38MAPK及p-p38MAPK蛋白表达。结果:在外周血和心肌组织中,与S组比较,I/R组、APS组、SB组、及APS+SB组中TNF-α、NF-κB、p-p38MAPK表达水平均明显升高(P值均小于0.05);与I/R组比较,APS组、SB组及黄芪APS+SB组中TNF-α、NF-κB和p-p38MAPK表达水平明显降低(P值均小于0.05)。APS+SB组对TNF-α、NF-κB、和p-p38的蛋白表达抑制作用要显著强于APS组的抑制作用(P值均小于0.05)。结论:黄芪多糖和p38MAPK阻断剂(SB203580)均能够有效改善未成年大鼠的心肌缺血再灌注损伤时的炎症反应,黄芪多糖和SB203580联用可以明显抑制TNF-α和NF-κB的表达,抑制p38MAPK信号通路,具有抑制心肌缺血再灌注损伤的协同作用。
Objective: To study the effect of astragalus polysaccharides on the inflammatory injury induced by myocardial ischemia-reperfusion in juvenile rats. Methods: One week old male SD rats were randomly divided into 5 groups: sham operation group (S group), ischemia / reperfusion group (I / R group), APS group (40 mg · kg -1) (APS + SB203580 group, APS 40 mg · kg -1 and SB203580 5 mg · kg -1) were treated with p38MAPK blocker SB203580 (5 mg · kg -1, SB) APS + SB group) .After administration for 20 days, the left anterior descending coronary artery was ligated for 60 min, then the blood was resuscitated for 120 min and the rats were sacrificed by orbital sampling.ELISA and Western- The expression of TNF-α, NF-κB, p38MAPK and p-p38MAPK protein in myocardium were measured.Results: In peripheral blood and myocardium, compared with S group, I / R group, APS group, SB group and APS + SB group TNF-α, NF-κB and p-p38MAPK in APS group, SB group and Astragalus APS + SB group were significantly higher than those in I / R group (P < κB and p-p38MAPK were significantly lower than those in APS group (all P values were less than 0.05) .APS + SB group had significantly more inhibitory effect on TNF-α, NF-κB and p-p38 protein than APS group P values were less than 0.05) .Conclusion: Astragalus polysaccharide and p38MAPK blocker (SB203580) can effectively improve the myocardium of juvenile rats When inflammation of blood reperfusion injury, APS, and may be combined with SB203580 significantly inhibit the expression of TNF-α and NF-κB, inhibition of p38MAPK signal transduction pathway, synergistic inhibition of myocardial ischemia-reperfusion injury.