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Characterization of kynurenine pathway in patients with diarrhea-predominant irritable bowel syndrome.
European Journal of Histochemistry ( IF 2.1 ) Pub Date : 2020-06-19 , DOI: 10.4081/ejh.2020.3132
Pingping Li 1 , Jimin Zheng 1 , Yun Bai 1 , Dingxin Wang 1 , Zijin Cui 1 , Yueqin Li 1 , Jian Zhang 1 , Yuzhen Wang 1
Affiliation  

Our objectives are to demonstrate whether the kynurenine pathway is activated in diarrhea-type irritable bowel syndrome (IBS-D) patients, and whether the neurotoxic metabolite quinolinic acid (QUIN) is out of balance with the neuroprotective metabolite kynurenic acid (KYNA), and further explore whether this can lead to increase of N-methyl D-aspartate receptor 2B (NMDAR2B) expression in the enteric nervous system and in turn leads to intestinal symptoms and mood disorders. All enrolled healthy controls and patients accepted IBS symptom severity scale (IBS-SSS) score, Self-rating Depression Scale (SDS) and Self-rating Anxiety Scale (SAS) anxiety and depression scores, and also underwent colonoscopy to collect ileum and colonic mucosa specimens. The expression of NMDAR2B in intestinal mucosa was detected by immunofluorescence, and fasting serum was collected to detect the tryptophan (Trp), kynurenine (KYN), KYNA and QUIN by high performance liquid chromatography tandem mass spectrometry (HPLC-MS/MS). Our results showed that the kynurenine pathway of IBS-D patients was activated. The production of QUIN and KYNA was imbalanced and resulting in an increased NMDAR2B for patients with IBS-D, which may be involved in intestinal symptoms and mood disorders of IBS-D.

中文翻译:

腹泻型肠易激综合征患者犬尿氨酸途径的特征。

我们的目标是证明腹泻型肠易激综合征(IBS-D)患者是否激活犬尿氨酸途径,以及神经毒性代谢物喹啉酸(QUIN)是否与神经保护性代谢物健尿酸(KYNA)失衡,以及进一步探讨这是否会导致肠道神经系统中N-甲基D-天冬氨酸受体2B(NMDAR2B)表达增加,进而导致肠道症状和情绪异常。所有入选的健康对照和患者均接受IBS症状严重程度量表(IBS-SSS)评分,自评抑郁量表(SDS)和自评焦虑量表(SAS)焦虑和抑郁评分,并接受结肠镜检查以收集回肠和结肠粘膜标本。免疫荧光检测NMDAR2B在肠粘膜中的表达,高效液相色谱串联质谱法(HPLC-MS / MS)收集空腹血清,检测色氨酸(Trp),犬尿氨酸(KYN),KYNA和QUIN。我们的结果表明,IBS-D患者的犬尿氨酸途径被激活。QUIN和KYNA的产生不平衡,导致IBS-D患者的NMDAR2B升高,这可能与IBS-D的肠道症状和情绪异常有关。
更新日期:2020-06-19
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