MiRNA-384-5p靶向GABRB1调节氯胺酮诱导的神经元神经毒性。

Pub Date : 2024-01-01 DOI:10.5137/1019-5149.JTN.36367-21.2

Qiange Yang, Feiyu Long

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引用次数: 0

摘要

目的氯胺酮是一种广泛应用于临床的麻醉辅助药物，可诱导大脑海马神经退行性变。微小RNA（miRNA）已被证明与氯胺酮介导的神经毒性的调节有关。本研究旨在确定miR-384-5p在氯胺酮诱导的神经毒性中的作用。材料和方法从大鼠身上分离海马神经元，并用不同剂量的氯胺酮处理。RT-qPCR用于测量氯胺酮处理的神经元中的miR-384-5p水平。MTT法检测神经元活力。TUNEL染色和流式细胞术检测神经元凋亡。利用H2-DCFDA染色检测细胞内ROS水平。使用蛋白质印迹法测量蛋白质水平。在HEK293T细胞中使用荧光素酶报告基因实验来验证miR-384-5p与GABRB1.RESULTSKetamine诱导的神经毒性和miR-384-5p在海马神经元中的上调的相互作用。MiR-384-5p下调通过抑制神经元凋亡和ROS活性来减轻氯胺酮诱导的神经毒性。GABRB1被证明是miR-384-5p靶向的。GABRB1耗竭加重了氯胺酮诱导的神经毒性。此外，GABRB1缺失降低了miR-384-5p抑制对氯胺酮介导的神经毒性的保护作用。结论MiR-384-5p通过靶向GABRB1调节氯胺酮诱导的海马神经元神经毒性。

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MiRNA-384-5p Targets GABRB1 to Regulate Ketamine-Induced Neurotoxicity in Neurons.

Aim: To determine the function of miR-384-5p in ketamine-induced neurotoxicity.

Material and methods: Neonatal hippocampal neurons were isolated from rats and treated with varying doses of ketamine. RT-qPCR was utilized to measure the miR-384-5p level in ketamine-treated neurons. Neuronal viability was evaluated by MTT assay. TUNEL staining and flow cytometry were applied to measure neuronal apoptosis. H2-DCFDA staining was utilized to detect the intracellular ROS level. Protein levels were measured using Western blotting. A luciferase reporter experiment was used in HEK293T cells to verify the interaction of miR-384-5p with GABRB1.

Results: Ketamine induced neurotoxicity and miR-384-5p upregulation in hippocampal neurons. miR-384-5p downregulation mitigated ketamine-induced neurotoxicity by restraining apoptosis and ROS activity in neurons. GABRB1 was demonstrated to be targeted by miR-384-5p. GABRB1 depletion worsened ketamine-induced neurotoxicity. Moreover, GABRB1 depletion lessened the protective effect of miR-384-5p inhibition against ketamine-mediated neurotoxicity.

Conclusion: miR-384-5p regulates ketamine-induced neurotoxicity in hippocampal neurons by targeting GABRB1.

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