摘要
目的:观察大鼠心肌缺血再灌注(M IR)时AngⅡ、ALD、IGF-1、ICAM-1和自由基代谢的变化及灯盏花素对其影响,探讨大鼠M IR损伤的机制。方法:SD大鼠30只,分为假手术对照(sham)组,M IR组和灯盏花素+M IR组,放免法检测血浆AngⅡ、ALD和血清IGF-1水平。免疫组织化学法检测心肌ICAM-1蛋白表达。检测血清、心肌组织SOD、MDA和GSH-PX及心肌线粒体Na+,K+-ATP酶、Mg2+-ATP酶、Ca2+-ATP酶活性。结果:与sham组相比,M IR组血浆AngⅡ、ALD明显升高,血清IGF-1含量明显降低;灯盏花素干预后血浆AngⅡ、ALD低于M IR组,血清IGF-1水平高于M IR组。与sham组相比,M IR组心肌线粒体Na+,K+-ATP酶、Mg2+-ATP酶、Ca2+-ATP酶活性明显下降;灯盏花素干预后心肌线粒体Na+,K+-ATP酶、Mg2+-ATP酶、Ca2+-ATP酶活性明显升高。与sham组相比,M IR组血清、心肌MDA明显升高,血清、心肌SOD和GSH-PX明显降低;灯盏花素干预后血清、心肌MDA低于M IR组,心肌SOD和GSH-PX水平高于M IR组。与sham组相比,M IR组心肌ICAM-1蛋白表达明显升高;灯盏花素干预后心肌ICAM-1蛋白表达低于M IR组。结论:AngⅡ、ALD增高和IGF-1减低可能共同参与了M IR的发生。M IR时存在自由基代谢异常,补充灯盏花素后,可通过提高SOD活性,增高GSH-PX水平,降低MDA含量,减轻脂质过氧化和自由基损伤,改善心肌组织功能。M IR时有大量ICAM-1蛋白表达,与心肌损伤关系密切。灯盏花素可通过减少ICAM-1蛋白表达,起到心肌保护作用。
Objective： To observe the effects of Breviscapine on the changes of angiotensin Ⅱ （ Ang Ⅱ ）, aldosterone（ALD）, Insulin-like growth factor-1 （ IGF-1 ）, the intercellular adhesion molecule-1 （ ICAM-1 ） and free radicals in ischemic reperfusion myocardium, and to investigate the mechanism of myocardial ischemic reperfusion injure. Methods： Thirty SD rats were divided into three groups with each group 10 rats （sham group, MIR group and Breviscapine group）. The changes of plasma Ang Ⅱ , ALD and serum IGF-1 were examined by BIA. The ICAM-1 protein expressions were evaluated by immunohistochemi method. The contents of malonialdehyde（MDA） in serum and myocardial tissues were detected. The activities of superoxide dismutase （SOD） and glutathione peroxidase （GSH-PX） in serum and myocardial tissues were measured. The activities of Na^ ＋, K^＋ -ATPase, Mg^2＋ -ATPase, Ca^2＋ -ATPase in myocardial mitochondria were measured. Results： Compared with sham group, the levels of Ang Ⅱ and ALD in plasma were increased significantly, the levels of serum IGF-1 were decreased significantly in MIR group. Compared with MIR group, the levels of Ang Ⅱ and ALD in plasma were decreased significantly, the levels of IGF-1 were increased significantly in Breviscapine group. Compared with sham group, the activities of Na^＋ , K^＋ -ATPase, Mg^2＋ -AT- Pase, Ca^2＋ -ATPase in myocardial mitochondria were decreased significantly in MIR group. Compared with MIR group, the activities of Na^＋ , K^＋ -ATPase, Mg^2＋ -ATPase, Ca^2＋-ATPase in myocardial mitochondria were increased significantly in Breviscapine group. Compared with sham group, the contents of MDA in serum and myocardium were increased significantly, the levels of SOD and GSH-PX in myocardium were decreased significantly in MIR group. Compared with MIR group, the levels of MDA in serum and myocardium were decreased significantly, the activities of SOD and GSH-PX in myocardium were increased significantly in Breviscapine group. Compared with sham group, the levels of ICAM-1 in myocardium were increased significantly in MIR group. Compared with MIR group, the levels of ICAM-1 in myocardium were decreased significantly in Breviscapine group. Conclusion： The findings indicated that Ang Ⅱ ALD and IGF-1 could participate myocardial ischemic reperfusion injure. The results also suggested that Breviscapine could relieve myocardial ischemic reperfusion injure induced by MIR, and this action was mediated by the reduction of the expression of ICAM-1 protein. Breviscapine had obvious protective effects on myocardial ischemic and reperfusion injury probably by scavenging hydroxyl free radicals, decreasing the level of plasma Ang Ⅱ and ALD, the level of MDA in serum and myocardium and increasing the level of serum IGF-1, the level of SOD and GSH-PX in myocardium, the level of Na^＋ , K ^＋ -ATPase, Mg^2＋ -ATPase, Ca^2＋ -ATPase in myocardial mitochondria.
出处
《江苏大学学报（医学版）》
CAS
2006年第6期477-480,484,共5页
Journal of Jiangsu University：Medicine Edition
基金
江苏大学青年自然科学基金(JDQ03029)
