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作 者:郑浩楠 张瑛[2,3,4] 迟雁 ZHENG Hao-Nan;ZHANG Ying;CHI Yan(Department of Gastroenterology,Peking University First Hospital,Beijing 100034,China;Neuroscience Research Institute;Department of Neurobiology,School of Basic Medical Sciences,Key Laboratory for Neuroscience;Ministry of Education/National Health Commission,Peking University,Beijing 100191,China)
机构地区:[1]北京大学第一医院消化科,北京100034 [2]北京大学神经科学研究所 [3]北京大学基础医学院神经生物学系 [4]教育部/国家卫生健康委员会神经科学重点实验室,北京100191
出 处:《中国疼痛医学杂志》2021年第2期113-118,共6页Chinese Journal of Pain Medicine
基 金:北京大学医学部“临床+X”合作项目(BMU2020MX004)。
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。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.
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