The Cardioprotective Effects of Aminoguanidine on Lipopolysaccharide Induced Inflammation in Rats
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The Cardioprotective Effects of Aminoguanidine on Lipopolysaccharide Induced Inflammation in Rats Farimah Beheshti1,2 · Mahmoud Hosseini1,3 · Milad Hashemzehi1,4 · Mohammad Reza Hadipanah4 · Maryam Mahmoudabady1,5
© Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Myocardial dysfunction, a major component of sepsis-induced multiorgan failure, contributes to the production of massive amounts of pro-inflammatory cytokines. Nitric oxide (NO) is known to act as a precursor of free radicals in inflammation. This research was conducted to assess the effect of aminoguanidine (AG) on lipopolysaccharide (LPS)-induced heart injury. 50 male rats were categorized into five groups (n = 10): (1) control, (2) LPS, (3) LPS-AG50, (4) LPS-AG100, and (5) LPSAG150. LPS (1 mg/kg) was injected for 5 weeks, and AG (50, 100 and 150 mg/kg) was injected 30 min prior to LPS administration. All drugs were injected intraperitoneally. LPS-evolved cardiovascular toxicity was indicated by the augmentation in the level of nitric oxide (NO) metabolites, interleukin (IL)-6 and malondialdehyde (MDA), as well as reduced contents of total thiol groups, catalase (CAT), and superoxide dismutase (SOD) activity in serum, heart, and aortic tissues. In AG treated groups, noxious effects of LPS were not observed in the serum and harvested tissues. AG reduced MDA, NO metabolites, and IL- 6 and increased total thiol, CAT, and SOD activity in the heart, aorta and serum. As an inhibitor of inducible NO synthase (iNOS), AG further reduced LPS-induced oxidative stress and inflammation, hence considered as cardioprotective. Keywords Lipopolysaccharide · Heart · Aminoguanidine · Oxidative stress · Inflammation
Introduction Heart failure, a last communal path of numerous cardiovascular diseases, is one of the primary causes of death worldwide. It encompasses sustained pressure overload (such as Communicated by Y. James Kang. * Maryam Mahmoudabady [email protected] 1
Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
2
Neuroscience Research Center, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran
3
Division of Neurocognitive Sciences, Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
4
Student Research Committee, Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
5
Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
hypertension), myocardial ischemia or infarction, volume overload (such as valvular heart disorders), and inherited or acquired cardiomyopathies. Inflammation and oxidative damage appear to be important causes involved in the progression of heart failure [1]. In the present research, lipopolysaccharide (LPS) was utilized to induce systemic inflammation. LPS is a key component of the outer membrane of Gram-negative bacteria. The immune system is continually exposed to low amo
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