Consequences of exercising on ischemia–reperfusion injury in type 2 diabetic Goto-Kakizaki rat hearts: role of the HO/NOS system

Diabetology & Metabolic Syndrome

Csaba Varga²  Anikó Pósa²  Zoltán Baráth¹  Anett Csonka²  Szilvia Török²  Amin Al Awar²  Médea Veszelka²  Renáta Szabó²  Krisztina Kupai² 

[1] Department of Orthodontics and Pediatric Dentistry, Faculty of Dentistry, University of Szeged, Szeged, 6720, Hungary;Department of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, Kozep fasor 52, Szeged, 6726, Hungary

关键词: Exercise;    Nitric oxide synthase;    Heme oxygenase;    Ischemia–reperfusion;   

Others  :  1229630
DOI  :  10.1186/s13098-015-0080-x

 received in 2015-04-10, accepted in 2015-09-24,  发布年份 2015

【 摘 要 】

Background

It is well established that physical exercise continues to be one of the most valuable forms of non-pharmacological therapy against diabetes mellitus; however, the precise mechanism remains unknown. The aim of this study was to investigate the cardioprotective effect of voluntary exercise in the Goto-Kakizaki type 2 diabetic rat heart against ischemia–reperfusion injury and to clarify its biochemical background, focusing on the nitric oxide synthase/heme oxygenase system.

Methods

One group of male Goto-Kakizaki rats were allowed voluntary exercise, whereas others were kept sedentary for 6 weeks. At the end of the 6th week the hearts were isolated from both groups and subjected to 45-min coronary occlusion followed by 120-min reperfusion. The infarct size was evaluated by means of triphenyltetrazolium chloride staining. The cardiac and aortic nitric oxide synthase/heme oxygenase activities, plasma leptin and glucose concentrations were also assessed.

Results

The sedentary state prior to the ischemia–reperfusion injury was associated with a significantly higher infarct size (24.56 ± 2.21 vs. 16.66 ± 1.87 %) as compared with that in the voluntary wheel-running group. Exercise altered the constitutive nitric oxide synthase activity; an enhancement was evident in the cardiac (42.5 ± 2.72 vs. 75.6 ± 13.34 pmol/min/mg protein) and aortic tissues (382.5 ± 66.57 vs. 576.9 ± 63.16 pmol/min/mg protein). Exercise lead to a higher heme oxygenase activity (0.68 ± 0.08 vs. 0.92 ± 0.04 nmol bilirubin/h/mg protein) in the diabetic rat hearts. Exercise was associated with lower plasma leptin (192.23 ± 7.22 vs. 169.65 ± 4.6 ng/L) and blood glucose (19.61 ± 0.76 vs. 14.58 ± 0.88 mmol/L) levels.

Conclusions

These results indicate the beneficial role of exercise against myocardial ischemia–reperfusion injury in diabetic rats. These observations in experimental diabetes suggest that the cytoprotective mechanism of exercise involves modulation of the nitric oxide synthase/heme oxygenase system and metabolic parameters that may be responsible for cardioprotection.

【 授权许可】

   
2015 Kupai et al.

【 图 表 】

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