Aim

We aim to study the anti-apoptotic effect of microRNA-21-5p (miR-21-5p) in the oxidative stress-induced apoptosis of Schwann cells and the relevant mechanism in this research, laying a foundation for the treatment of peripheral neuropathy (PNP).

Methods and materials

The oxidative stress model was established by using hydrogen peroxide (H₂O₂). ROS level were detected by DCFH-DA (2,7-Dichlorodi-hydrofluorescein diacetate). Western blot and fluorescence staining were used to detect the apoptosis and autophagy level. The miR-21-5p overexpression model was established by transfection of miR-21-5p mimics into RSC96 cells. Five groups of control group, H₂O₂ group, H₂O₂ + chloroquine (CQ) group, H₂O₂ + miR-21-5p mimics group, and H₂O₂ + miR-21-5p mimics+rapamycin (RAPA) group were included in our experiment.

Key findings

Compared with control group, miR-21-5p was decreased in H₂O₂-treated RSC96 cells, while autophagy and apoptosis were both promoted. The result revealed that apoptosis was probably triggered by activation of autophagy in H₂O₂-treated group. In order to verify the relationship between autophagy and apoptosis more accurately, we used CQ to inhibit autophagy. Compared with H₂O₂-treated group, autophagy and apoptosis were both weakened in H₂O₂ + CQ group. Subsequently, we found the antiapoptotic effect of miR-21-5p in this model, overexpression of miR-21-5p prevented cells from being damaged by oxidative stress, it induced the decrease of PTEN and the level of autophagy, leading to decreased level of apoptosis.

Significance

The identified relationship between miR-21-5p, apoptosis, and autophagy promotes us to find a new mechanism to improve the treatment for PNP.

中文翻译：

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microRNA-21-5p的过表达通过抑制自噬而阻止了氧化应激诱导的RSC96细胞凋亡。

目标

我们旨在研究microRNA-21-5p（miR-21-5p）在氧化应激诱导的雪旺氏细胞凋亡中的抗凋亡作用及其相关机制，为治疗周围神经病变奠定基础（ PNP）。

方法和材料

采用过氧化氢（H ₂ O ₂）建立了氧化应激模型。通过DCFH-DA（2，7-二氯二氢荧光素二乙酸酯）检测ROS水平。Western blot和荧光染色检测细胞凋亡和自噬水平。通过将miR-21-5p模拟物转染到RSC96细胞中，建立了miR-21-5p过表达模型。对照组分为5组：H ₂ O ₂组，H ₂ O ₂  +氯喹（CQ）组，H ₂ O ₂  + miR-21-5p模拟组和H ₂ O ₂  + miR-21-5p模拟组+雷帕霉素（RAPA）组包括在我们的实验中。

主要发现

与对照组相比，H ₂ O ₂处理的RSC96细胞中miR-21-5p降低，而自噬和细胞凋亡均得到促进。结果表明，H ₂ O ₂处理组细胞凋亡可能是由自噬激活引起的。为了更准确地验证自噬与细胞凋亡之间的关系，我们使用了CQ抑制自噬。用H相比₂ ö ₂处理组，自噬和细胞凋亡都H中减弱₂ ö ₂ + CQ组。随后，我们在该模型中发现了miR-21-5p的抗凋亡作用，miR-21-5p的过度表达可防止细胞受到氧化应激的破坏，从而诱导PTEN的降低和自噬水平的降低，从而导致其水平下降。细胞凋亡。

意义

miR-21-5p，细胞凋亡和自噬之间的确定关系促使我们寻找改善PNP治疗的新机制。