Effect of agmatine on experimental vascular endothelial dysfunction

Area of Science:

• Cardiovascular Science
• Pharmacology
• Toxicology

Background:

• Nicotine (NIC) induces vascular endothelial dysfunction (VED) and oxidative stress.
• VED is characterized by impaired nitric oxide production and increased inflammation.
• Agmatine sulfate (AG) is investigated for its potential protective effects.

Purpose of the Study:

• To investigate the efficacy of agmatine sulfate (AG) in mitigating nicotine (NIC)-induced vascular endothelial dysfunction (VED) in a rabbit model.
• To elucidate the underlying mechanisms of AG's protective effects against NIC-induced VED.

Main Methods:

• Rabbits were administered nicotine (NIC) for 6 weeks to induce VED, with or without co-administration of agmatine sulfate (AG).
• Evaluated serum lipid profiles, markers of oxidative stress (TBARS, reduced glutathione, SOD), nitric oxide metabolites (nitrite/nitrate), VCAM-1, and aortic NF-κB levels.

Main Results:

• Agmatine sulfate (AG) significantly improved serum lipid profiles.
• AG treatment prevented NIC-induced vascular endothelial dysfunction (VED) and attenuated oxidative stress.
• AG administration led to a significant reduction in serum VCAM-1 and aortic NF-κB levels.

Conclusions:

• Agmatine sulfate (AG) demonstrates protective effects against nicotine (NIC)-induced vascular endothelial dysfunction (VED).
• AG mitigates VED by reducing oxidative stress, decreasing VCAM-1 expression, and inhibiting NF-κB activation.
• AG improves vascular endothelial integrity, suggesting therapeutic potential for VED.