Dexmedetomidine alleviates high glucose-induced podocyte damage by inhibiting EDA2R

Abstract

Purpose: To investigate the effect and mechanism of action of dexmedetomidine (Dex) on podocyte injury.
 Methods: Cells were incubated with high glucose (50 mM) to induce a podocyte injury model in vitro. Cell viability, apoptosis, the expression of related protein related in podocyte injury and albumin permeability were evaluated by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT), flow cytometry, western blot and Transwell assays.
 Results: Dex administration enhanced HG-induced cell viability and the relative protein expression of Bcl-2, but reduced the HG-induced relative protein level of Bax and apoptosisrate in podocytes (p < 0.05). Besides, Dex incubation compensated HG-induced relative protein expressions of nephrin and podocin in podocytes but did the reverse with regard to relative protein expression of desmin and albumin permeability (p < 0.05). Moreover, Dex treatment resulted in a decrease in ectodysplasin A2 receptor (EDA2R) expression in HG-induced podocytes. The level of EDA2R was upregulated by the transfection of overexpression plasmid containing the EDA2R sequences. Overexpression of EDA2R reversed Dex-induced increase in cell viability, apoptosis, expression of nephrin, podocin and desmin, as well as albumin permeability in HG-stimulated podocytes (p < 0.05).
 Conclusion: Dex ameliorates HG-induced podocyte injury via inhibition of EDA2R, indicating that Dex is a potential alternative drug for the treatment of podocyte injury.

Effect of dexmedetomidine on convalescence quality after general anesthesia and postoperative delirium, and on cognitive function in elderly patients undergoing lower limb surgery

“…Dexmedetomidine, an alpha-2 adrenergic receptor agonist, exerts anti-sympathetic and sedative effects and is widely used in perioperative period of surgery [4,5]. Dexmedetomidine is an alpha-2 adrenoceptor agonist that produces sedative, stress-reducing, and analgesic effects by reducing sympathetic nervous system activity.…”