Resveratrol attenuates the inflammatory reaction induced by ischemia/reperfusion in the rat heart

被引：40

作者：

Cong, Xiaoqiang ^{[1
,2
]}

Li, Ying ^{[3
]}

Lu, Na ^{[1
]}

Dai, Yajian ^{[4
]}

Zhang, Huijie ^{[4
]}

Zhao, Xin ^{[1
]}

Liu, Ya ^{[2
]}

机构：

[1] Jilin Univ, Bethune Hosp 1, Dept Cardiol, Changchun 130021, Jilin, Peoples R China

[2] Jilin Univ, Sch Publ Hlth, Dept Nutr & Toxicol, Changchun 130021, Jilin, Peoples R China

[3] Peoples Hosp Jilin Prov, Dept Emergericy Internal Med, Changchun 130021, Jilin, Peoples R China

[4] Friendship Hosp Linjiang, Dept Internal Med, Linjiang 134600, Jilin, Peoples R China

来源：

MOLECULAR MEDICINE REPORTS | 2014年 / 9卷 / 06期

关键词：

resveratrol; ischemia/reperfusion injury; neutrophil; tumor necrosis factor-alpha; ISCHEMIA-REPERFUSION INJURY; NECROSIS-FACTOR-ALPHA; MYOCARDIAL-ISCHEMIA; NITRIC-OXIDE; SIRT1; PREVENTION; APOPTOSIS; CHEMOKINE; PROTECTS; SYNTHASE;

D O I：

10.3892/mmr.2014.2090

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The role of resveratrol (Res) in inflammation induced by ischemia/reperfusion is not well understood. The aim of the present study was to investigate whether Res modulates neutrophil accumulation and tumor necrosis factor-alpha (TNF-alpha) induction in an ischemia/reperfusion-injured rat heart model. The rats were randomly exposed to sham surgery, myocardial ischemia/reperfusion (MI/R) alone, MI/R + Res, MI/R + Res + L-NG-nitroarginine methyl ester (L-NAME) and MI/R + Res + methylene blue (MB). The results demonstrated that compared with MI/R, Res reduced the myocardial infarct area, myocardial myeloperoxidase levels, serum creatinine kinase and lactate dehydrogenase levels, and serum and myocardial TNF-alpha production. All the effects of Res demonstrated were inhibited by L-NAME (a nitric oxide (NO) synthase inhibitor) and MB [a cyclic guanosine monophosphate (cGMP) inhibitor]. Thus, Res produces cardioprotective and anti-inflammatory effects. These effects may be associated with an increase in NO production, the inhibition of neutrophil accumulation, TNF-alpha induction and cGMP signaling pathways in myocardium subjected to MI/R.

引用

页码：2528 / 2532

页数：5

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