Protective Mechanism of NLRP3 Inflammatory Bodies Mediated by Dexmedetomidine on Renal Injury in Rats with Hemorrhagic Shock

Objectives: to investigate the protective mechanism of NLRP3 inflammatory bodies mediated by Dexmedetomidine (DEX) on renal injury in rats with hemorrhagic shock. Materials and Methods: 18 healthy SD rats were divided into control (group A), model (group B) and right metomidine (group C) group. Group B and C were used to establish the model of hemorrhagic shock by improved Wiggers method. After successful modeling, the group B was injected intravenously with normal saline 5 μg kg-1 h-1. The patients in group C were given DEX 5 μg kg-1·h-1 intravenously. The mean arterial pressure of 60 min was recorded before shock, after shock and after resuscitation. Serum Creatinine (SCR) and BUN were measured by biochemical analyzer. The NLRP3, Caspase-1, IL-18 and IL-1 β in serum of rats were detected by ELISA method. The protein of NLRP3, Caspase-1 and Kim-1 were detected by Western blot. Results: The MAP after shock and resuscitation (30, 60 min) in the group B and C were reduced than group A. The indexes of SCR and BUN in the group B was increased than group A. The contents of serum NLRP3, Caspase-1, IL-18, IL-1 β and Kim-1 in the group B was increased than group A, while these in the group B was decreased than group A. The protein levels of NLRP3, Caspase-1 and Kim-1 in the group C was decreased than group B. Conclusion: DEX can reduce the renal injury induced by hemorrhagic shock in rats and has a protective effect on the kidney. The mechanism may be achieved by inhibiting the inflammatory bodies of NLRP3 and then reducing the expression of inflammatory factors and Kim-1.