MiR-30b-5p alleviates trigeminal neuralgia induced by chronic constriction injury of the infraorbital nerve by regulating the voltage-gated sodium channel Nav1.3 in rats

IF 2.5 4区医学 Q3 NEUROSCIENCES

Neuroscience Letters Pub Date : 2025-04-01 DOI:10.1016/j.neulet.2025.138223

Tingting Hu , Mengci Shao , Jiajia Liu , Xiaorong Yan , Liecheng Wang , Yuanyin Wang , Wenhua Xu

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引用次数: 0

Abstract

Nav1.3 is a tetrodotoxin-sensitive voltage-gated sodium channel isoform encoded by SCN3A, the abnormal expression of which plays a crucial role in the generation of ectopic discharge, as well as being associated with allodynia and hyperalgesia. Using bioinformatics analysis, we showed that miR-30b-5p directly targets SCN3A. We aimed to explore whether miR-30b-5p can participate in trigeminal neuralgia (TN) in rats by regulating the expression of Nav1.3. The rat TN model was constructed through infraorbital nerve-chronic constriction injury (ION-CCI), which was verified by measuring the change in mechanical threshold and the expression of activating transcription factor 3 (a marker of nerve damage) in the trigeminal ganglia (TG). The expression of miR-30b-5p in postoperative TG was downregulated, whereas that of Nav1.3 was upregulated in rats subjected to ION-CCI. Overexpression of miR-30b-5p repressed the expression of Nav1.3 in TG and alleviated ION-CCI-induced TN. MiR-30b-5p targets to regulate the expression of SCN3A, thereby reducing or aggravating TN. Therefore, miR-30b-5p may be a novel therapeutic target for neuropathic pain.

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来源期刊

Neuroscience Letters 医学-神经科学

CiteScore

5.20

自引率

0.00%

发文量

408

审稿时长

50 days

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