Dexmedetomidine improves propofol-induced neuronal injury in rat hippocampus with the involvement of miR-34a and the PI3K/Akt signaling pathway
This study was designed to explore the mechanisms of DEX in the propofol-induced neuronal injury in rat hippocampus.Materials and methodsRat hippocampi were treated with propofol, and then neuronal injury, neuronal apoptosis, PSD95 and apoptosis-related protein expression in CA1 region were measured after DEX administration and/or ant-miR-34a. miR-34a expression was detected using RT-qPCR, while the binding of miR-34a and Sirtuin1 (SIRT1) was identified with dual luciferase reporter gene assay, and the activation of PI3K/Akt signaling pathway was detected. Additionally, hippocampal neurons were cultured in vitro and treated with DEX and propofol. The viability and apoptosis of hippocampal neurons, fluorescence intensity of Ca2+ and neuronal morphology were detected.Key findingsIn vivo experiments, propofol induced obvious neuronal injury in rat hippocampus, while DEX at different doses reduced hippocampal neuronal apoptosis and miR-34a expression but increased PSD95 expression in rat hippocampus. Low expression of miR-34a reduced propofol-induced neuronal injury by targeting SIRT1 and activating the PI3K/Akt pathway. In vitro experiments, propofol induced neuronal injury, which was alleviated by DEX treatment, accompanied with increased neuronal viability, but decreased apoptosis and fluorescence intensity of Ca2+. The attenuation of neuronal injury achieved by DEX was impaired by over-expression of miR-34a. Meanwhile, over-expression of SIRT1 in neurons with overexpressed mi...
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ConclusionsImplantation of spinal cord stimulation electrodes through a surgical laminectomy using dexmedetomidine is a safe and feasible procedure with adequate comfort for patient and surgeon. This way of working increases the optimal position of the electrode resulting in the most convenient stimulation pattern and avoiding revisions.
Publication date: Available online 19 February 2020Source: Pharmacology Biochemistry and BehaviorAuthor(s): Aaron Ettenberg, Kathy Ayala, Jacob T. Krug, Lisette Collins, Matthew S. Mayes, Matthew P.A. FisherAbstractSub-anesthetic doses of ketamine produce an increase in rodent ambulation that is attenuated by co-administration of naturally-occurring lithium (LiN), the drug most commonly employed in the treatment of bipolar illness. As a consequence, ketamine-induced hyperactivity has been proposed as an animal model of manic behavior. The current study employed a modified version of this model to compare the potency of LiN...