Dexmedetomidine ameliorates the inflammatory immune response in rats with acute kidney damage

It has been demonstrated that dexmedetomidine (Dex) can protect patients with acute kidney injury from experiencing further tissue damage, however its mechanism of action remains unclear. The present study investigated the immune modulatory functions of Dex in rats with acute kidney injury (AKI) induced via injection of lipopolysaccharide into the tail vein. ELISA analysis showed that Dex reduced the levels of inflammatory cytokines in rats with AKI in a dose dependent manner. Furthermore, the regulatory effects of Dex on cytokine production disappeared when the α-2 adrenergic receptor antagonist Yohimbine (YOH) was added. For a detailed investigation on how Dex regulates the immune response in rats with AKI, the impact of Dex on the viability of splenocytes and lymphocytes was determined and it was determined that Dex did not influence splenocyte and lymphocyte viability. In addition, ELISA tests showed that Dex regulated the production of the T-helper (Th) 17 cytokines interleukin (IL)-17 and IL-23, but not the Th1 cytokine tumor necrosis factor α, in splenocytes and lymphocytes. To confirm whether Dex functioned as an α-2-adrenergic receptor in these immune regulations, YOH was administered together with Dex. When Dex and YOH were administered together, the regulatory functions of Dex were reduced, confirming that Dex acted as an agonist on the α-2-adrenergic receptor. Thus the results of the current study may provide novel insights regarding how Dex modulates immune functions in AKI.