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心肌缺血/再灌注损伤后血清和心肌中瘦素水平的变化

[Changes of leptin levels in serum and myocardium after myocardial ischemia/reperfusion injury].

作者信息

Xue Hui, Yan Guang-tao, Lin Ji, Hao Xiu-hua, Zhang Kai

机构信息

Research Laboratory of Biochemistry, Basic Medical Institute, General Hospital of PLA, Beijing 100853, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2009 May;25(2):221-3.

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 established, serum 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 reperfusion, which recovered to the level before injury (8.38 +/- 2.56) ng/ml, 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 reperfusion.

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.

摘要

目的

探讨大鼠心肌缺血/再灌注损伤对血清及心肌中瘦素水平的影响,并探讨瘦素在心肌缺血/再灌注损伤中的作用。

方法

建立大鼠心肌缺血/再灌注损伤模型,检测血清乳酸脱氢酶(LDH)和瘦素水平,分别采用苏木精-伊红染色和免疫组织化学法观察心肌组织病理学变化及瘦素表达。

结果

缺血再灌注组血清LDH显著升高(P<0.05),提示模型成功建立且诱导了一定程度的局部心肌损伤。缺血组血清瘦素水平为(6.34±2.49)ng/ml,显著低于对照组(7.50±2.93 ng/ml,P<0.05)。再灌注后瘦素水平逐渐恢复,再灌注2 h时达到(8.32±1.74)ng/ml,恢复至损伤前水平(8.38±2.56)ng/ml,并随再灌注时间延长呈升高趋势。免疫组织化学结果显示,与假手术组相比,其他四组心肌瘦素蛋白表达均显著降低(P<0.01),并按缺血45 min/再灌注1 h、缺血45 min/再灌注3 h、缺血45 min和缺血45 min/再灌注2 h的顺序降低。

结论

心肌缺血/再灌注损伤后早期45 min血液中瘦素水平显著降低,心肌中瘦素表达也显著降低。心肌病理损伤与瘦素变化可能存在一定关系。

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