【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;然而,与基础状态相比较,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。更多还原

【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） was used to detect the visceral sensitivity after the establishment of IBS model. Open field test and elevated plus maze were used to evaluate the anxiety level of 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, compared with the basal condition, 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.更多还原