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饮食中的迪奥斯基宁转录下调肠道NPC1L1表达,以防止小鼠胆固醇胆结石的形成
Weiyi Shen1, Wentao Shao1,2,3, Qihan Wang1
1Center of Gallstone Disease, Shanghai East Hospital, and Institution of Gallstone Disease, School of Medicine, Tongji University, Shanghai, China.
Journal of biomedical science
|June 27, 2023
概括
迪奥斯基宁 (DG) 通过抑制肠道胆固醇的吸收,完全防止胆固醇在小鼠中的胆结石形成. 这种天然化合物通过降低NPC1L1表达和调节肠道微生物群来降低胆固醇负担.
科学领域:
- 生物化学 生化学
- 胃肠病学 胃肠病学
- 药理学 药理学是指药理学的学科.
背景情况:
- 胆固醇胆结石病很普遍,需要采取减少胆固醇负担的策略.
- 迪奥斯基宁 (DG) 正在研究其防止胆结石形成的潜力.
- 了解胆固醇代谢是治疗胆结石疾病的关键.
研究的目的:
- 在小鼠模型中研究迪奥斯基宁 (DG) 预防胆固醇胆结石形成的疗效.
- 阐明DG影响胆固醇吸收和代谢的分子机制.
- 评估DG对肠道微生物群的影响及其在胆结石预防中的作用.
主要方法:
- 成年雄性C57BL/6J小鼠在8周内接受了带或不带DG或ezetimibe的石化食 (LD).
- 分析了胆结石发生率,肠道和肝脏脂质含量以及胆固醇代谢基因表达.
- 使用Caco2细胞和小鼠模型研究DG对胆固醇吸收,NPC1L1表达,STAT3激活和肠道微生物群的影响.
主要成果:
- 石化饮食诱导了100%的胆结石形成;DG和ezetimibe完全阻止了它.
- 通过降低小鼠和Caco2细胞NPC1L1表达的调节,DG抑制了肠道胆固醇的吸收.
- DG抑制了STAT3酸化,调节了肠道微生物群,并减少了LPS诱导的STAT3激活和NPC1L1表达.
结论:
- 饮食中的二氧化基因 (DG) 有效地防止胆固醇胆结石的形成.
- 通过减少NPC1L1表达,DG抑制了肠道胆固醇的吸收.
- 总局的机制涉及STAT3信号通路调节和肠道微生物群的改变.
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