Apelin protect against multiple organ injury following hemorrhagic shock and decrease the inflammatory response

INTRODUCTION: Hemorrhagic shock (HS) result in multiple organ injury and inflammatory response that lead to death. The exact mechanism is not clear. Apelin is an endogenous ligand of orphan G-protein coupled receptor APJ. Apelin has anti-inflammatory effects on the release of inflammatory mediators. OBJECTIVES: To examine the protective effects of apelin against multiple organ injury and the possible involvement of inflammatory pathways. METHODOLOGY: Male Sprague-Dawley rats (300–350 g) were subjected to hemorrhage over 60 min to reach a mean arterial blood pressure of 40 mmHg. Then, rats were treated or not with 1 mL of 10 nm/L apelin-13 intraarterially resuscitation was performed in vivo by the reinfusion of the shed blood for 30 min to restore normotension. Blood samples were collected for measurement of tumor necrosis factor (TNF) using ELISA (R and D systems). Biopsies were obtained from organs for light microscopic examination. RESULTS: HS rats showed significant increase the levels of TNF. Apelin significantly lowered the production of TNF-α. Histological examination of hemorrhagic shocked untreated rats revealed structural damage. Less histological damage was observed in the organs of treated rats. Apelin-treatment decreased the number of inflammatory cells and mitochondrial swollen in cells. CONCLUSION: Treatment with apelin before resuscitation protects against multiple organ injury in HS by attenuation the inflammatory response and might be a therapeutic target for HS.