RESUMO
Growth hormone-releasing hormone antagonists (GHRHAnt) have been associated with antitumor and antioxidative activities. The present study investigates for the first time the effects of those compounds towards pro-inflammatory cytokine expression in a murine model of cecal ligation and puncture (CLP) - induced sepsis. The results indicate that GHRHAnt JV-1-36 significantly suppressed IL-1α, IL-6, and pSTAT3 activation in septic lungs. Moreover, GHRHAnt treatment reduced bronchoalveolar lavage fluid (BALF) protein concentration, suggesting a protective effect of that compound in sepsis-induced lung edema. Based on those findings, it is suggested that GHRHAnt may represent an exciting new therapeutic possibility in sepsis-induced endotoxemia and lung injury.
RESUMO
P53 represents the paradigm of a multitalented transcription factor, responsible for the cellular defense against a plethora of potentially harmful stimuli. It exercises the ability to strongly oppose both cancer and inflammation, partially due to the fact that both conditions are highly interrelated. Endothelium hyperpermeability is considered the hallmark of severe lung inflammation, and the cardinal feature of the lethal acute respiratory distress syndrome. An emerging body of evidence suggests a strategic role of P53 towards vascular barrier integrity. The "endothelium defender" orchestrates meticulously devised responses; to counteract toxin-induced destructions of endothelium monolayers. The present effort seeks to further our understanding on the expanding P53 universe, discussing the most recent information regarding the involvement of that molecule in the pulmonary function.
