Атеросклероз и сахарный диабет 2-го типа имеют ряд общих патогенетических механизмов, что позволило рассматривать метаболический компонент в качестве эквивалента типового механизма современной патологии. Применение препаратов, являющихся регуляторами нейроиммуноэндокринной системы, которые ответственны за экспрессию белков, принимающих участие в регуляции иммунитета - один из наиболее перспективных подходов к решению этой проблемы.
Chronic low-grade inflammation is a significant factor in the development of obesity associated diabetes. The purpose of the present study was to investigate the anti-inflammatory effects of metformin (lidocaine) and the related molecular mechanisms. In light of these findings, we suggest that metformin (lidocaine) attenuates the LPS-induced expression of proinflammatory and adhesion molecule by inhibiting NF-kappaB activation. The received results testify to ability of metformin (lidocaine) to decrease adhesion and modulation of apoptosis and PMN free oxygen radicals production. It was established that the inflammation development was accompanied with pronounced proatherogenic blood lipid and lipoprotein metabolism disturbances in association with insulin resistance, hyperglycemia. The drugs' effect: the inhibition of lipid metabolism observed in all lipid fractions (i.e. free cholesterol, free fatty acids, triglycerides. Lidocaine is a commonly used local anaesthetic agent which has also been found to possess anti-inflammatory activity in several disorders. Lidocaine has been reported to attenuate the inflammatory response in addition to its anesthetic activity.