tailieunhanh - Báo cáo y học: "Salivary gland derived peptides as a new class of anti-inflammatory agents: review of preclinical pharmacology of C-terminal peptides of SMR1 protein"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Salivary gland derived peptides as a new class of anti-inflammatory agents: review of preclinical pharmacology of C-terminal peptides of SMR1 protein. | Mathison et al. Journal of Inflammation 2010 7 49 http content 7 1 49 JOURNAL OF INFLAMMATION REVIEW Open Access Salivary gland derived peptides as a new class of anti-inflammatory agents review of preclinical pharmacology of C-terminal peptides of SMR1 protein Ronald D Mathison1 Joseph S Davison1 A Dean Befus2 Daniel A Gingerich3 Abstract The limitations of steroidal and non steroidal anti-inflammatory drugs have prompted investigation into other biologically based therapeutics and identification of immune selective anti-inflammatory agents of salivary origin. The traditional view of salivary glands as accessory digestive structures is changing as their importance as sources of systemically active immunoregulatory and anti-inflammatory factors is recognized. Salivary gland involvement in maintenance of whole body homeostasis is regulated by the nervous system and thus constitutes a neuroendocrine axis . The potent anti-inflammatory activities both in vivo and in vitro of the tripeptide Phe-Glu-Gly FEG are reviewed. FEG is a carboxyl terminal peptide of the prohormone SMR1 identified in the rat submandibular salivary gland The D-isomeric form feG mimics the activity of its L-isomer FEG. Macropharmacologically feG attenuates the cardiovascular and inflammatory effects of endotoxemia and anaphylaxis by inhibition of hypotension leukocyte migration vascular leak and disruption of pulmonary function and intestinal motility. Mechanistically feG affects activated inflammatory cells especially neutrophils by regulating integrins and inhibiting intracellular production of reactive oxygen species. Pharmacodynamically feG is active at low doses 100 pg kg and has a long 9-12 hour biological half life. As a therapeutic agent feG shows promise in diseases characterized by over exuberant inflammatory responses such as systemic inflammatory response syndrome and other acute inflammatory diseases. Arthritis sepsis acute pancreatitis asthma acute .

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