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Expression of mRNA of TLR2, TLR4 in dynamics in patients with ret | 8266
Pancreatic Disorders & Therapy

Pancreatic Disorders & Therapy
Open Access

ISSN: 2165-7092

+44 1478 350008

Expression of mRNA of TLR2, TLR4 in dynamics in patients with retroperitoneal pancreatogenic phlegmon


International Conference on Pancreatic Disorders and Treatment

October 17-19, 2016 Chicago, USA

Mikhail Agapov

Moscow State University, Russia

Posters & Accepted Abstracts: Pancreat Disord Ther

Abstract :

Acute pancreatitis is a common clinical condition. Excessive systemic inflammatory response syndrome (SIRS) in acute pancreatitis leads to distant organ damage and multiple organ dysfunction syndromes (MODS), which is the primary cause of morbidity and mortality in this condition. Development of in vivo experimental models of acute pancreatitis and associated systemic organ damage has enabled us to study the role played by inflammatory mediators in the pathogenesis of acute pancreatitis and associated systemic organ damage. Using these models, recent studies have established the critical role played by inflammatory mediators in acute pancreatitis and the resultant MODS. Hydrogen sulfide (H2S) plays an important role in cardiovascular, central nervous and gastrointestinal systems and has been shown to act as a vasodilator. We have also shown that H2S acts as a mediator of inflammation. Substance P is 11 amino-acid neuropeptide that is released from nerve endings in many tissues. Subsequent to its release, substance P binds to neurokinin-1 (NK-1) receptors on the surface of effector cells. Using experimental models, recent studies in our laboratory have established the critical role played by H2S and substance P in acute pancreatitis. Furthermore, early results point to the clinical relevance of this research. Studies with experimental animal models of disease will therefore help define the role of these mediators in the pathogenesis of acute pancreatitis and can lead to the development of novel therapeutic approaches for this condition.

Biography :

Email: getinfo911@mail.ru

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