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Anatol J Cardiol. 2017 Nov;18(5):315-320. doi: 10.14744/AnatolJCardiol.2017.7952.

Protection by nitrite against the ischemic effects induced by acute myocardial infarction in mice.

Author information

1
Department of Preventative Medicine, School of Medicine Ningbo University, Ningbo-People's Republic of China. zhaojinshun@nbu.edu.cn.

Abstract

OBJECTIVE:

This research was aimed to investigate the correct dose of nitrite that would act as a protection against the ischemic effects induced by acute myocardial infarction (AMI).

METHODS:

Mice were randomly divided into a sham-operation group (sham), an AMI operation group (AMI), and a nitrite pretreatment+AMI operation group (N+AMI). Seven days before the AMI operation, mice in the N+AMI group were pretreated with sodium nitrite in drinking water.

RESULTS:

One week after the AMI operation, serum lactate dehydrogenase (LDH) and creatine kinase (CK) activities in both AMI and N+AMI group were significantly higher than those in the sham group, but there were no significant differences between AMI and N+AMI mice. Contents of inducible nitric oxide synthase (iNOS) in the noninfarct area of the left ventricle in the N+AMI mice were significantly higher than those in the AMI mice, with no difference in the infarct area. Coagulation necrosis in the cardiomyocytes was observed in both AMI and N+AMI mice; however, it was less severe in the N+AMI mice. Western blot analyses showed that nitrite pretreatment resulted in up-regulation of antiapoptotic factors Bcl-2 and p21waf1/cip1 signal proteins, but down-regulation of the proapoptotic factor Bax signal protein. Furthermore, nitrite pretreatment also showed significant alleviation of AMI-induced signal protein expressions of inflammatory factors of NF-K B and oxidative factors of Hsp 70 and HO-1.

CONCLUSION:

These results suggest that nitrite show certain protective effects against the ischemic effects induced by AMI in mice, which might be attributed to the synthesis of NO induced by iNOS through up-regulation of antiapoptotic factors and down-regulation of proapoptotic and inflammatory factors.

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