在癫痫大鼠模型中，迷走神经刺激通过调节miR-210影响炎症反应和抗凋亡反应。
Vagus nerve stimulation affects inflammatory response and anti-apoptosis reactions via regulating miR-210 in epilepsy rat model.
作者信息
Bie Bizhou, Wang Zhizhong, Chen Yingchun, Sheng Liuqing, Li Huanhuan, You Huichao, Ye Jianfeng, Zhang Qing, Li Jun
机构信息
Department of Neurosurgery, The Third People's Hospital of Hubei Province, Wuhan, Hubei, China.
出版信息
Neuroreport. 2021 Jun 9;32(9):783-791. doi: 10.1097/WNR.0000000000001655.
BACKGROUND
Studies have shown that vagus nerve stimulation (VNS) significantly reduces the frequency of seizures. MicroRNAs (miRNAs) in cerebrospinal fluid are expected to become a new biomarker of epilepsy. Therefore, studying the interaction mechanism between the VNS and miRNAs is hopeful of bringing a new therapeutic direction for the treatment of epilepsy.
METHODS
Kainic acid was used to induce the Sprague-Dawley rat epilepsy model, and the rats were treated with VNS. The miR-210 expression was determined by quantitative reverse transcription PCR (qRT-PCR). Racine score was adopted to evaluate the performance of behavioral seizures, whereas qRT-PCR and ELISA were employed to test inflammatory factors. Western blotting was implemented to testify the inflammatory and apoptotic proteins.
RESULTS
Kainic acid-induced the Sprague-Dawley rat epilepsy model and upregulated the expression of miR-210, inflammatory response, inflammation and apoptosis-related proteins in brain tissues. In addition, compared with the epilepsy model group, miR-210 in the hippocampus of the epilepsy model rats treated with VNS was downregulated, and the expression of apoptosis-related proteins and inflammatory factors was reduced. Moreover, after further inhibiting the expression of miR-210, the inhibition of VNS on epilepsy, inflammation and apoptosis were significantly enhanced.
SUMMARY
VNS relieves the inflammatory response and apoptosis of epileptic rats via inhibiting miR-210.
背景
研究表明，迷走神经刺激（VNS）可显著降低癫痫发作频率。脑脊液中的微小RNA（miRNA）有望成为癫痫的新型生物标志物。因此，研究VNS与miRNA之间的相互作用机制有望为癫痫治疗带来新的治疗方向。
方法
用 kainic 酸诱导 Sprague-Dawley 大鼠癫痫模型，并用 VNS 对大鼠进行治疗。通过定量逆转录 PCR（qRT-PCR）测定 miR-210 的表达。采用 Racine 评分评估行为性癫痫发作表现，同时用 qRT-PCR 和 ELISA 检测炎症因子。通过蛋白质印迹法验证炎症和凋亡相关蛋白。
结果
kainic 酸诱导 Sprague-Dawley 大鼠癫痫模型，并上调脑组织中 miR-210 的表达、炎症反应、炎症和凋亡相关蛋白。此外，与癫痫模型组相比，接受 VNS 治疗的癫痫模型大鼠海马中的 miR-210 下调，凋亡相关蛋白和炎症因子的表达降低。此外，在进一步抑制 miR-210 的表达后，VNS 对癫痫、炎症和凋亡的抑制作用显著增强。
总结
VNS 通过抑制 miR-210 减轻癫痫大鼠的炎症反应和凋亡。
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