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作 者:王国华[1] 钟爱梅[2] 孙宗全[1] 夏家红[1] 刘金平[1] 柳祎[1] 冯剑锷[1]
机构地区:[1]华中科技大学同济医学院附属协和医院心血管外科,武汉430022 [2]河南省人民医院整形外科
出 处:《中华胸心血管外科杂志》2009年第3期187-189,共3页Chinese Journal of Thoracic and Cardiovascular Surgery
基 金:本课题受国家自然基金项目资助(30471715)
摘 要:目的探讨脂氧素A4对心肌缺血再灌注损伤的保护作用及可能机制。方法30只雄性昆明小鼠,随机分为缺血再灌注组(A组),脂氧素A4(LXA4)处理组(B组)和LXA4+ZnPP[血红素氧合酶(HO)-1抑制剂]处理组(C组),每组10只。建立小鼠缺血再灌注模型,再灌注30min后各组分别经颈总动脉插管注入同体积的10%无水乙醇、LXA4、LXA4+ZnPP,5h后测定各组血清中的TNF-α、CK及LDK,心肌组织中髓过氧化物酶(MPO)活性、丙二醛(MDA)含量,TUNEL法检测心肌细胞凋亡率及病理切片观测心肌炎性细胞浸润。结果与A组比较,B组心肌炎性细胞浸润减少,CK、LDH及MPO活性、TNF-α浓度、MDA含量及心肌凋亡率均显著降低(P〈0.01),而ZnPP可以显著减弱LXA4的保护作用(P〈0.05)。结论LXA4对心肌缺血再灌注损伤具有保护作用,HO-1可能在LXA4的心肌保护作用中起重要作用。Objective To investigate the roles of lipoxin A4, an endogenous lipid mediator with wide anti-inflammatory features, in attenuating myocardial isehemia-reperfusion injury and the possible mechanisms. Methods Thirty male KM mice were divided randomly into three groups, 10 in each: ischemia-reperfusion group (group A), lipoxin A4 (0.1 mg/kg) group (group B) and Zn- PP (Zinc protoporphyrin IX, 25 mg/kg) plus lipoxin A4 (0.1 mg/kg) group ( group C). A isehemia-repeffusion heart model was developed by ligating the left anterior descending branch of the coronary artery. A dose of 10% dehydrated alcohol in 0.2 ml for group A, a dose of isochorie lipoxin A4 for group B and a dose of isochorie ZrPP + lipoxin A4 for group C was infused into the ascending aorta through a catheter, which was passing the right common carotid artery, 30 minutes after reperfusion. The cencentration of serum TNF-α, activities of serum ereatine kinase(CK) and lactate dehydrogenase (LDH), activities of myeloperoxidase (MPO) and malondialdehyde (MDA) and the cell apoptosis rate in the myocardial tissue were measured 5 hours after repeffnsion. Pathological features of the inflammatory infiltration in the myocardium were also obsarvated. Results As cempared with group A, the inflammatory infiltration in the ischemie and necrotic regions of the myocardium was reduced, with group C in the intermediate range. The serum activities of CK and LDH were significantly lower in group B and C than that in group A, and the lowest activities were detected in group B. Similar findings were observed for MPO, an indicator for neutrophil infiltration, and MDA, an indicator for cell injury caused by oxygen radicals, in the myocardium. The concentration of TNF-α and the rate of cadioeyte apoptesis were decreased significantly in group B( P 〈 0.01 ). ZnPP, an inhibitor of heine oxygenase ( HO)-1, attenuated the above protective effects of lipoxin A4 significantly (P 〈 0.05). Conclusion Lipoxin A4 has protecti
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