Turkish neurosurgery · 2022
Expression and Role of CXCL13 and MiR-186-5p in the Trigeminal Ganglion of a Rat Model of Trigeminal Neuralgia.
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Feng Linfei, Yang Liangxin, Shi Xiufang, Wang Liecheng, Wang Yuanyin
Аннотация
AIM: To reveal the roles of CXCL13 and miR-186-5p in a rat model (adult male Sprague-Dawley rats, 7?8 weeks old, 180?200 g) of trigeminal neuralgia (TN) established via chronic constriction injury of the infraorbital nerve (ION-CCI).
MATERIAL AND METHODS: The results of behavioural tests and the expression levels of miR-186-5p and CXCL13 in the trigeminal ganglion (TG) were compared between the sham and ION-CCI groups, as well as the consequences of the miR-186-5p mimic and inhibitor.
RESULTS: Compared with the sham-operated rats, ION-CCI rats displayed mechanical hypersensitivity in the von Frey hair test. Western blotting revealed the upregulation of CXCL13 and downregulation of miR-186-5p in the TG of ION-CCI rats relative to their expression in sham rats. Furthermore, an miR-186-5p mimic decreased CXCL13 protein levels and increased the mechanical withdrawal thresholds of ION-CCI rats. CXCL13 protein levels also increased after the injection of an miR-186-5p inhibitor. Finally, miR-186-5p was found to be expressed in the TG and was downregulated in ION-CCI rats compared to sham rats.
CONCLUSION: miR-186-5p may negatively regulate CXCL13 to influence the occurrence and development of TN. Collectively, our findings shed new light on novel therapies for the treatment of TN.
MATERIAL AND METHODS: The results of behavioural tests and the expression levels of miR-186-5p and CXCL13 in the trigeminal ganglion (TG) were compared between the sham and ION-CCI groups, as well as the consequences of the miR-186-5p mimic and inhibitor.
RESULTS: Compared with the sham-operated rats, ION-CCI rats displayed mechanical hypersensitivity in the von Frey hair test. Western blotting revealed the upregulation of CXCL13 and downregulation of miR-186-5p in the TG of ION-CCI rats relative to their expression in sham rats. Furthermore, an miR-186-5p mimic decreased CXCL13 protein levels and increased the mechanical withdrawal thresholds of ION-CCI rats. CXCL13 protein levels also increased after the injection of an miR-186-5p inhibitor. Finally, miR-186-5p was found to be expressed in the TG and was downregulated in ION-CCI rats compared to sham rats.
CONCLUSION: miR-186-5p may negatively regulate CXCL13 to influence the occurrence and development of TN. Collectively, our findings shed new light on novel therapies for the treatment of TN.