V. Ivanov, S. Ivanova, M.W. Roomi, T. Kalinovsky, A. Niedzwiecki, M. Rath
Research Communications in Molecular Pathology and Pharmacology 2004
Recognition of the involvement of inflammatory processes in atherosclerotic lesion initiation and development of pathological consequences initiated a search for an effective inhibitor. Naturally occurring compounds demonstrate a wider spectrum of biological activity and fewer side effects than synthetic drugs. Mixtures of natural compounds often produce synergistically enhanced therapeutic action.
This prompted us to investigate whether a unique nutrient mixture (NS), containing ascorbic acid, lysine, proline, arginine, N-acetyl cysteine and tea phenolics, could reduce an autocrine response of human aortic smooth muscle cell (SMC) to inflammatory stimuli. Cultured SMC were challenged with tumor necrosis factor-alpha (TNF_) or lipopolysaccharide (LPS) in the presence or absence of NS. Expression of leading mediators of inflammatory reaction was assayed with ELISA (R&D Systems).
2.5-fold induction of interleukin-1alpha (IL-1_) content in cellular media was completely reversed in the presence of 20 _g/ml NS (containing 20 _M ascorbic acid). Secretion of pro-interleukin–1 beta (pro-IL-1_) and of its activator, caspase-1, was inhibited by 46% and 67%, respectively. This resulted in significant reduction of IL-1_ formation. Secretion of interleukin-6 (IL-6) and interleukin-8 (IL-8) was also dramatically reduced. Moreover, addition of NS significantly inhibited expression of cell adhesion molecules: sP-selectin and monocyte chemoattractant protein-1 (42% and 65% inhibition, respectively). Anti-inflammatory effects of NS exceeded the sum of actions of its individual components.
From these data we conclude that the mixture of ascorbic acid, tea phenolics, and selected amino acids tested has a strong potential against involvement of vascular cells into inflammatory response to pathogens.
atherosclerosis, cytokines, interleukin, inflammatory mediators, inflammation, nutrient synergy, human aortic SMC
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