Why the study?
Does agmatine sulfate prevent nicotine-induced vascular endothelial dysfunction in rabbits?
Does agmatine sulfate prevent nicotine-induced vascular endothelial dysfunction in rabbits?
Agmatine sulfate may protect against nicotine-induced vascular endothelial dysfunction by reducing oxidative stress and inflammation markers in a rabbit model.
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Rationale for human trials of agmatine in nicotine-exposed patients; hypothesis-generating from rabbit data and should not change practice.
This study was designed to investigate the effect of agmatine sulfate (AG, CAS2482-00-0) in nicotine (NIC)-induced vascular endothelial dysfunction (VED) in rabbits. NIC was administered to produce VED in rabbits with or without AG for 6 weeks. Serum lipid profile, serum thiobarbituric acid reactive substances, reduced glutathione, superoxide dismutase generation, serum nitrite/nitrate, serum vascular cellular adhesion molecule-1 (VCAM-1), and aortic nuclear factor κB (NF-κB) levels were analyzed.Treatment with AG markedly improves lipid profile and prevented NIC-induced VED and oxidative stress. The mechanism of AG in improving NIC-induced VED may be due to the significant reduction in serum VCAM-1 levels and aortic NF-κB. Thus, it may be concluded that AG reduces the oxidative stress, nitric oxide production, VCAM-1 levels, and aortic NF-κB expression, thereby consequently improving the integrity of vascular endothelium.
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Nader et al. (2015) studied this question.
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