数据日期 2026-10-29 · 生成时间 2026-10-29 06:03
研究问题
However, how changes in gut 5-HT signaling affect the disease development mechanism of IBS is still unclear.
方法
This study received approval from the Institutional Animal Care and Use Committee at Ludong University on 22 June 2024 (Authorization Permit Number: LDU-IRB20240622).；The animal experiments were conducted in accordance with the guidelines outlined in the People’s Republic of China National Standard GB/T 35892–2018 [15] for the ethical review of laboratory animal welfare.；Animal Treatments] All experimental animals were female C57BL/6J mice aged 6–7 weeks, purchased from Vital River Laboratory Animal Technology Co., Ltd.；Mice were housed under specific pathogen-free (SPF) conditions with a 14 h light/dark cycle and had ad libitum access to standard rodent feed and filtered water during the entire experimental period.
核心结论
结论：We further demonstrated that this pathway mediated restraint stress–induced inhibition of NLRP6 inflammasome and autophagy, leading to impaired goblet cell function and disruption of the intestinal mucosal barrier.
局限
This study has several noteworthy limitations for translational interpretation.；First, all in-vivo animal experiments were performed exclusively in female C57BL/6J mice; given known sex-based disparities in irritable bowel syndrome prevalence [34], the observed regulatory cascade may not fully recapitulate signaling events in male organisms.；Second, mechanistic evidence largely relies on pharmacological interventions using PCPA and SB-269970, which carry potential off-target effects; future genetic-editing studies are required to confirm cell-type-specific functions of this signaling axis.
对本项目的价值
★★☆☆☆ 方法学进展决定我们能否在有限样本下检出真实效应，属基础设施级收益。最大样本量约 120。
全文来源
PMC JATS 全文（正文 42,603 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：Psychological Stress Disrupts Goblet Cell Function and Intestinal Barrier via 5-HT/HTR7-Mediated NLRP6 and Autophagy Suppression.
- 期刊与标识：Biology (Basel) · PMID 42939471 · DOI 10.3390/biology15201870**
B 级证据分级：B 级（同行评议临床前研究，主要为动物模型）
本文核心结论来自动物模型或体外细胞学，属临床前证据，不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义，与人类临床结局之间仍有距离。
关于本文的文献来源：本站依据 IMA 知识库「五刊监控·深度文献卡片」撰写，依据已获取的期刊全文（方法、样本量与结论已回到原文核对）；未能获取全文的同批条目另行标注「摘要级」，全程未做任何数值推算补全。