Abstract

Purpose

Sevoflurane is a widely used anesthetics, however, it has been reported that sevoflurane has neurotoxic effects. Studies have shown that miR-221-3p can ameliorate neuron damage. This study was to investigate whether miR-221-3p could reduce the neurotoxic effect of sevoflurane on nerve cells.

Materials and methods

The rat hippocampal neuron cells were treated with sevoflurane or cultured normally. And we constructed neuron cells that overexpressed or low expression of miR-221-3p in the presence or absence of sevoflurane. The cells were transfected with CDKN1B or siCDKN1B, and co-transfected with miR-221-3p mimic and CDKN1B or miR-221-3p inhibitor and siCDKN1B. Cell viability and apoptosis were detected by CCK-8 and flow cytometer. Target gene of miR-221-3p were predicted by TargetScan and luciferase reporter assay. The expressions of related genes were detected by western blotting and quantitative real-time polymerase chain reaction.

Results

Sevoflurane decreased miR-221-3p level and increased CDKN1B level, inhibited cell viability and promoted apoptosis. Overexpress of miR-221-3p decreased CDKN1B level, up-regulated cell viability and inhibited apoptosis, and reversed the effects of sevoflurane on cell viability and apoptosis, while the effects low expression of miR-221-3p was contrary. CDKN1B was the target gene of miR-221-3p, which inhibited cell viability and promoted apoptosis, and reversed the effects of miR-221-3p mimic, whereas siCDKN1B did the opposite effects.

Conclusions

Sevoflurane can cause nerve cell injury, and miR-221-3p may promote cell activity and inhibit apoptosis by inhibiting CDKN1B expression, thereby ameliorating cell injury induced by sevoflurane.

中文翻译：

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miR-221-3p对七氟醚所致神经细胞损伤的改善作用研究

摘要

目的

七氟醚是一种广泛使用的麻醉剂，但据报道七氟醚具有神经毒性作用。研究表明，miR-221-3p 可以改善神经元损伤。本研究旨在探讨 miR-221-3p 是否可以降低七氟醚对神经细胞的神经毒性作用。

材料和方法

大鼠海马神经元细胞用七氟醚处理或正常培养。我们构建了在存在或不存在七氟醚的情况下过表达或低表达 miR-221-3p 的神经元细胞。用CDKN1B或siCDKN1B转染细胞，并用miR-221-3p模拟物和CDKN1B或miR-221-3p抑制剂和siCDKN1B共转染。CCK-8和流式细胞仪检测细胞活力和凋亡。通过 TargetScan 和荧光素酶报告基因分析预测 miR-221-3p 的靶基因。通过蛋白质印迹和定量实时聚合酶链反应检测相关基因的表达。

结果

七氟醚降低 miR-221-3p 水平并增加 CDKN1B 水平，抑制细胞活力并促进细胞凋亡。过表达miR-221-3p降低CDKN1B水平，上调细胞活力并抑制细胞凋亡，并逆转七氟醚对细胞活力和细胞凋亡的影响，而miR-221-3p低表达的影响则相反。CDKN1B 是 miR-221-3p 的靶基因，抑制细胞活力并促进细胞凋亡，并逆转 miR-221-3p 模拟物的作用，而 siCDKN1B 则相反。

结论

七氟醚可引起神经细胞损伤，miR-221-3p可通过抑制CDKN1B表达促进细胞活性，抑制细胞凋亡，从而改善七氟醚诱导的细胞损伤。