ArticleExperimental and therapeutic medicine2017
Dexmedetomidine ameliorates the inflammatory immune response in rats with acute kidney damage.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Research status and advances in dexmedetomidine for sepsis‑induced multiple organ dysfunction syndrome (Review).International journal of molecular medicine · 2025Review
- The effects of Dexmedetomidine on Recovery from Acute KIdney INjury (DRAIN): a single-center retrospective review using the Medical Information Mart for Intensive Care, fourth edition (MIMIC-IV).Therapeutic advances in drug safety · 2025Article
- Dexmedetomidine activates the PKA/CREB pathway and inhibits proinflammatory factor expression through β2 adrenergic receptors.Immunity, inflammation and disease · 2024Article
- Tailored Therapeutic Doses of Dexmedetomidine in Evolving Neuroinflammation after Traumatic Brain Injury.Neurocritical care · 2022Article
- Dexmedetomidine Inhibits Neuroinflammation by Altering Microglial M1/M2 Polarization Through MAPK/ERK Pathway.Neurochemical research · 2020Article
- Dexmedetomidine improves cardiac function and protects against maladaptive remodeling following myocardial infarction.Molecular medicine reports · 2019Article
- Dexmedetomidine Promotes SH-SY5Y Cell Resistance Against Impairment of Iron Overload by Inhibiting NF-κB Pathways.Neurochemical research · 2019Article
- Dexmedetomidine Attenuates Orthotopic Liver Transplantation-Induced Acute Gut Injury viaOxidative medicine and cellular longevity · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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