TRPV1通过非焦虑依赖的机制参与肠易激综合征内脏高敏感的形成

TRPV1 Contributes to Visceral Hypersensitivity in Irritable Bowel Syndrome model induced by TNBS in a Non-anxiety-dependent Mechanism

摘要:

目的：探讨TRPV1受体是否通过影响焦虑水平，参与肠易激综合征（irritable bowel syndrome, IBS）内脏高敏感性的产生。 方法：通过三硝基苯磺酸（trinitrobenzene sulfonic acid, TNBS）单次灌肠的方法，分别使用野生型（wild type, WT）与Trpv1-/-小鼠构建IBS内脏高敏感小鼠模型；利用结直肠扩张-腹壁撤回反射（CRD-AWR）法，检测IBS模型鼠的内脏敏感性；利用旷场实验、高架十字迷宫实验检测小鼠焦虑水平。 结果：Trpv1-/-小鼠基础状态和IBS造模后的焦虑水平均低于野生型小鼠；本研究中TNBS单次灌肠构建的IBS模型未影响WT和Trpv1-/小鼠的焦虑水平；但IBS模型构建后的比较显示Trpv1-/-小鼠较WT小鼠的内脏高敏感性降低。 结论：在单次注射TNBS诱导的IBS模型中，TRPV1受体可能通过非焦虑依赖的机制参与IBS内脏高敏感的产生。

Abstract:

Objective: To investigate whether TRPV1 receptor contributes to the visceral hypersensitivity in irritable bowel syndrome (IBS) through affecting the anxiety level. Methods: Wild-type (WT) and Trpv1-/- mice were used to establish the IBS visceral hypersensitivity model by singular intrarectal administration of trinitrobenzene sulfonic acid (TNBS). Colorectal distension-abdominal withdrawal reflex (CRD-AWR) method was used to detect the visceral sensitivity after the establishment of IBS model. Open field test and elevated plus maze were used to evaluated the anxiety level of the mice. Results: The anxiety level of Trpv1-/- mice was reduced compared with the WT mice both in the basal condition and in IBS model. However, the anxiety levels of both Trpv1-/- mice and WT mice were unchanged after the establishment of IBS model. Trpv1-/- mice show reduced visceral hypersensitivity in IBS model compared with the WT mice. Conclusion: In singular intrarectal administration of TNBS-induced IBS model, TRPV1 receptors may contributes to IBS visceral hypersensitivity through a non-anxiety-dependent mechanism.