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Copyright (c) 2023 Chunyuan Lu, Nan Zhao
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Mechanism of Fat Emulsion-mediated PTEN-PI3K-AKT Signaling Pathway on Neurotoxicity of Bupivacaine
Corresponding Author(s) : Chunyuan Lu
Cellular and Molecular Biology,
Vol. 69 No. 2: Issue 2
Abstract
This study was to explore the application value of chromosome ten (PTEN) - phosphatidylinositol 3-kinase (PI3K) - protein kinase B (AKT) signaling pathway in the treatment of Bupivacaine toxicity to neuronal cells under the regulation of fat emulsion. Neurons in the hippocampus of newborn rats were treated with Bupivacaine and fat emulsion and divided into five groups. The activity and action potential of neurons in each group were measured and Nissl’s staining was performed. The results showed that the neuron activity of Bupivacaine group (42.36 ± 5.48%), Bupivacaine + fat emulsion group (70.23 ± 3.66%), and Bupivacaine + fat emulsion + PTEN/PI3K/AKT inhibitor group (79.28 ± 5.14%) was lower than that of the blank group (99.95 ± 3.42%). The duration of action potential in Bupivacaine group was increased (5.19 ± 0.48ms) and the frequency of action potential was decreased (13.87 ± 1.95) compared with the blank group (2.44 ± 0.37ms, 19.59 ± 2.14). The duration of the fat emulsion group (2.39 ± 0.39ms, 19.76 ± 2.05), Bupivacaine + fat emulsion group (2.88 ± 0.52ms, 18.53 ± 1.66), and Bupivacaine + fat emulsion + PTEN/PI3K/AKT inhibitor group (3.43 ± 0.69ms, 17.57 ± 1.58) was decreased, but the number of times increased (P < 0.05). In short, the fat emulsion can reverse the toxic effects of Bupivacaine on rat hippocampal neurons by regulating the PTEN/PI3K/AKT signaling pathway. This study provided a reference for the clinical treatment of the neurotoxicity of Bupivacaine.
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