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[大鼠心脏的心肌多胺代谢与缺血再灌注损伤]

[Myocardial polyamine metabolism and the ischemia-reperfusion injury in the rat heart].

作者信息

Han Li-ping, Xu Chang-qing, Jiang Chun-ming, Li Hong-zhu, Zhao Ya-jun, Gong Yong-sheng, DU You-ai, Guo Yi-min

机构信息

Department of Pathophysiology, Harbin Medical University, Harbin 150086, China.

出版信息

Zhonghua Xin Xue Guan Bing Za Zhi. 2008 Apr;36(4):346-9.

Abstract

OBJECTIVE

To observe the polyamines metabolism changes in rat cardiomyocytes underwent ischemia-reperfusion (I/R) injury.

METHODS

A branch of the descending left coronary artery was occluded to induce rat myocardial I/R injury (30 min ischemia followed by 2 h, 6 h, 12 h, and 24 h reperfusion). RT-PCR and Western blot were performed to detect the expression of spermidine/spermine N1-acetyltransferase (SSAT) and ornithine decarboxylase (ODC), the concentrations of polyamines were measured with high performance liquid chromatography in hearts with or without I/R.

RESULTS

The myocardial transcription and expression of SSAT and ODC were significantly upregulated. Compared with the sham group, ODC mRNA and SSAT mRNA respectively increased 3.1 fold and 3.8 fold and their proteins respectively increased 3.1 fold and 2.9 fold at 24 h of reperfusion (P < 0.01); the concentrations of spermidine, spermine and the total polyamine pool respectively decreased by 33.6%, 35.3% and 32.9% while putrescine concentration increased by 58.9% at 24 h of reperfusion (P < 0.01).

CONCLUSION

Our results suggest that ischemia-reperfusion in the heart may affect polyamine metabolism and the disturbance of polyamine metabolism might thus play a critical role in myocardial I/R injury in this model.

摘要

目的

观察大鼠心肌细胞缺血再灌注(I/R)损伤时多胺代谢的变化。

方法

结扎左冠状动脉分支诱导大鼠心肌I/R损伤(缺血30分钟,再灌注2小时、6小时、12小时和24小时)。采用逆转录聚合酶链反应(RT-PCR)和蛋白质免疫印迹法(Western blot)检测亚精胺/精胺N1-乙酰基转移酶(SSAT)和鸟氨酸脱羧酶(ODC)的表达,用高效液相色谱法测定有或无I/R心脏中多胺的浓度。

结果

心肌中SSAT和ODC的转录和表达显著上调。与假手术组相比,再灌注24小时时ODC mRNA和SSAT mRNA分别增加3.1倍和3.8倍,其蛋白分别增加3.1倍和2.9倍(P<0.01);再灌注24小时时,亚精胺、精胺和总多胺池浓度分别下降33.6%、35.3%和32.9%,而腐胺浓度增加58.9%(P<0.01)。

结论

我们的结果表明,心脏缺血再灌注可能影响多胺代谢,多胺代谢紊乱可能在该模型的心肌I/R损伤中起关键作用。

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