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心肌缺血/再灌注损伤后血清和心肌组织Leptin水平的变能
引用本文:Xue H,Yan GT,Lin J,Hao XH,Zhang K. 心肌缺血/再灌注损伤后血清和心肌组织Leptin水平的变能[J]. 中国应用生理学杂志, 2009, 25(2): 221-223
作者姓名:Xue H  Yan GT  Lin J  Hao XH  Zhang K
作者单位:解放军总医院基础所生化室,北京100853
基金项目:国家自然科学基金(30670821)
摘    要:目的:观察大鼠心肌缺血/再灌注损伤对血清和心肌组织瘦素(Leptin)表达的影响,探讨Leptin在心肌缺血/再灌注损伤中的作用。方法:建立大鼠心肌缺血/再灌注模型,检测血清乳酸脱氢酶(LDH)和Leptin浓度,并用HE染色和免疫组织化学观察心肌组织病理学及Lepfin表达水平。结果:缺血组、再灌注组血清LDH水平显著升高(P〈0.05),表明该模型制作成功,造成心肌局部一定程度的损伤。缺血组血清Leptin含量(6.34±2.49)ng/ml显著低于对照组(7.50±2.93ng/ml,P〈0.05);再灌注后Leptin水平缓慢恢复,于再灌注2h时Leptin达到(8.32±1.74)ng/ml,恢复到损伤前水平(8.38±2.56)ng/ml,且随再灌注时间延长有升高趋势。免疫纽化显示与假手术纽心肌Leptin蛋白表达水平相比,其他四组均有显著降低(P〈0.01),按缺血45min后再灌注1h组、缺血45min后再灌注3h组、单纯缺血45min组、缺血45min后再灌注2h组依次递减。结论:Leptin在心肌缺血/再灌注损伤后早期45min血中有明显减少,心肌组织中也明显表达下降。心肌组织病理损伤与Leptin的改变可能有一定的关系。

关 键 词:瘦素  缺血/再灌注损伤  心肌  乳酸脱氢酶

Changes of leptin levels in serum and myocardium after myocardial ischemia/reperfusion injury
Xue Hui,Yan Guang-tao,Lin Ji,Hao Xiu-hua,Zhang Kai. Changes of leptin levels in serum and myocardium after myocardial ischemia/reperfusion injury[J]. Chinese journal of applied physiology, 2009, 25(2): 221-223
Authors:Xue Hui  Yan Guang-tao  Lin Ji  Hao Xiu-hua  Zhang Kai
Affiliation:Research Laboratory of Biochemistry, Basic Medical Institute, General Hospital of PLA, Beijing 100853, China.
Abstract:Aim: To explore the effect of rat myocardial ischemia/reperfusion injury on leptin levels in serum and myocardium, and discuss the role of leptin in myocardial ischemia/reperfusion injury. Methods: A myocardial ischemia/reperfusion injury model of rats was estabilished, senan lactate dehydrogenase(LDH) and leptin levels were detected, and histopathological changes and leptin expressions in myocardium were investigated by hematoxylin-eosin staining and immunohistochemistry, respectively. Results: Serum LDH of ischemia and reperfusion groups increased significantly(P 〈 0.05), suggesting the model was successfully established and a certain degree of local myocardial injury was induced. Serum leptin of ischemia group(6.34 ± 2.49) ng/ml was significantly lower than control group(7.50 ± 2.93 ng/ml, P 〈 0.05). Leptin levels recovered gradually after reperfusion, reached(8.32 ± 1.74)ng/ml at 2 h after repeffusion, which recovered to the level before injury (8.38 ± 2.56)ng/nd, and showed a trend to increase as reperfusion time was elongated. Immunohistochemistry results showed that as compared with sham-operation group, myocardial leptin protein expressions of the other four groups were all significantly lower( P 〈 0.01 ), and decreased in order by 45 min ischemia/1 h reperfusion, 45 min ischemia/3 h reperfusion, 45 min ischemia and 45 min ischemia/2 h reperfu±sion. Conclusion: Leptin level in the blood decreases significantly at the early 45 min after myocardial ischemia/reperfusion injury, and its expression in myocardium also decreases significantly. There may be a certain relationship between the pathological injury of myocardium and the changes of leptin.
Keywords:leptin  ischemia/repfersion injury  myocardium  lactate dehydrogenase
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