Electroacupuncture Alleviates 46-Trinitrobenzene Sulfonic Acid-Induced Visceral Pain via the Glutamatergic Pathway in the Prefrontal Cortex.

Electroacupuncture Alleviates 46-Trinitrobenzene Sulfonic Acid-Induced Visceral Pain via the Glutamatergic Pathway in the Prefrontal Cortex.
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电针刺减轻了46-三硝基苯磺酸诱导的内脏疼痛,可通过前额叶皮层中的谷氨酸能途径进行内脏疼痛。

DOI:
10.1155/2023/4463063
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发表时间:
2023
影响因子:
--
通讯作者:
Xu, Maosheng
Xu, Maosheng
中科院分区:
生物学2区
文献类型:
--
作者:
Jiang, Hao;Li, Rongrong;Zhang, Fan;Zhou, Feini;Lin, Jiangnan;Kong, Ning;Chen, Haitao;Guo, Lingnan;Ye, Chenxiao;Li, Fuhao;Xu, Maosheng

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炎症性肠病(IBD)引起的内脏疼痛大大降低了受影响患者的生活质量。然而,IBD如何导致内脏疼痛的机制目前尚未完全了解。以往的研究表明,中枢神经系统(CNS)和肠-脑轴(GBA)在IBD引起的内脏痛中起重要作用。电针作为IBD的治疗方法之一,在临床上已被用于治疗各种类型的疼痛和胃肠道疾病。然而,电针是否通过肠-脑轴减轻IBD内脏痛尚未得到证实。为了验证内脏痛与CNS之间的关系,进行了以下实验。对从IBD大鼠模型获得的前额叶皮层(PFC)组织进行1H-NMR分析,以确定代谢物之间的联系及其在EA治疗内脏痛中的作用。采用Western blot法检测谷氨酸转运体兴奋性氨基酸转运体2(EAAT 2)和谷氨酸受体N-甲基-D-天冬氨酸(NMDA)的含量,验证电针治疗是否能减轻谷氨酸异常升高所致的神经毒性症状。研究结果表明,TNBS诱导的IBD大鼠PFC中谷氨酸含量显著增加。电针治疗后,这种变化被逆转。这一过程与EAAT2表达增加和PFC中NMDA受体表达减少有关。此外,观察到肠道谷氨酸代谢细菌增加。总之,这项研究表明,EA治疗可以减轻内脏疼痛,减少谷氨酰胺毒性PFC,并提供了一个替代的临床效用。
Visceral pain caused by inflammatory bowel disease (IBD) greatly diminishes the quality of life in affected patients. Yet, the mechanism of how IBD causes visceral pain is currently not fully understood. Previous studies have suggested that the central nervous system (CNS) and gut-brain axis (GBA) play an important role in IBD-inducing visceral pain. As one of the treatments for IBD, electroacupuncture (EA) has been used to treat various types of pain and gastrointestinal diseases in clinical practice. However, whether EA relieves the visceral pain of IBD through the gut-brain axis has not been confirmed. To verify the relationship between visceral pain and CNS, the following experiments were conducted. 1H-NMR analysis was performed on the prefrontal cortex (PFC) tissue obtained from IBD rat models to determine the link between the metabolites and their role in EA treatment against visceral pain. Western blot assay was employed for detecting the contents of glutamate transporter excitatory amino acid transporters 2 (EAAT2) and the glutamate receptor N-methyl-D-aspartate (NMDA) to verify whether EA treatment can alleviate neurotoxic symptoms induced by abnormal increases of glutamate. Study results showed that the glutamate content was significantly increased in the PFC of TNBS-induced IBD rats. This change was reversed after EA treatment. This process was associated with increased EAAT2 expression and decreased expression of NMDA receptors in the PFC. In addition, an increase in intestinal glutamic-metabolizing bacteria was observed. In conclusion, this study suggests that EA treatment can relieve visceral pain by reducing glutamine toxicity in the PFC, and serves an alternative clinical utility.
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