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Alginate oligosaccharide alleviates myocardial reperfusion injury by inhibiting nitrative and oxidative stress and endoplasmic reticulum stress-mediated apoptosis

Authors Guo JJ, Xu FQ, Li YH, Li J, Liu X, Wang XF, Hu LG, An Y

Received 18 May 2017

Accepted for publication 18 July 2017

Published 18 August 2017 Volume 2017:11 Pages 2387—2397


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Anastasios Lymperopoulos

Jun-Jie Guo,1,* Feng-Qiang Xu,2,* Yong-Hong Li,1,* Jian Li,1 Xin Liu,3 Xiao-Fan Wang,1 Long-Gang Hu,4 Yi An1

1Department of Cardiology, The Affiliated Hospital of Qingdao University, 2Department of Cardiology, Qingdao Municipal Hospital, 3Department of Geriatric Medicine, The Affiliated Hospital of Qingdao University, 4Department of Cardiology, The Affiliated Cardiovascular Hospital of Qingdao University, Qingdao, People’s Republic of China

*These authors contributed equally to this work

Abstract: Alginate oligosaccharide (AOS) has recently demonstrated the ability to protect against acute doxorubicin cardiotoxicity and neurodegenerative disorders by inhibiting oxidative stress and endoplasmic reticulum (ER) stress-mediated apoptosis, which are both involved in myocardial ischemia/reperfusion (I/R) injury. In the present study, we investigated whether pretreatment with AOS protects against myocardial I/R injury in mice and explored potential cardioprotective mechanisms. AOS pretreatment significantly decreased the infarct size, reduced the cardiac troponin-I concentration, and ameliorated the cardiac dysfunction. Accompanied with the reduced cardiac injury, AOS pretreatment clearly decreased I/R-induced myocardial apoptosis. With regard to mechanism, AOS pretreatment markedly attenuated nitrative/oxidative stress, as evidenced by decreases in 3-nitrotyrosine content and superoxide generation, and downregulated inducible nitric oxide synthase, NADPH oxidase2, and 4-hydroxynonenal. Moreover, AOS pretreatment decreased myocardial apoptosis by inhibiting the ER stress-mediated apoptosis pathway, which is reflected by the downregulation of C/EBP homologous protein, glucose-regulated protein 78, caspase-12, and Bcl-2-associated X protein, and by the upregulation of the anti-apoptotic protein B-cell lymphoma-2. Collectively, these findings demonstrate that AOS renders the heart resistant to I/R injury, at least in part, by inhibiting nitrative/oxidative stress and ER stress-mediated apoptosis.

alginate oligosaccharide, myocardial ischemia/reperfusion injury, nitrative/oxidative stress, endoplasmic reticulum, cardioprotection

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