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在老鼠中,阿特拉提利诺酸III通过PI3K/AKT/NF-κB/iNOS通路改善了反流性食道炎
Xianzhe Si1, Weijie Lin1, Zhiyao Chen1
1Department of Gastrointestinal & Esophageal Surgery, The 2nd Affiliated Hospital of Fujian Medical University, Quanzhou, China.
Heliyon
|November 13, 2023
概括
阿特拉提利诺利德III (ATLIII) 通过减少炎症和氧化应激,有效地治疗大鼠的反流性食道炎 (RE). 这种天然化合物通过调节PI3K/AKT/NF-κB/iNOS通路而起作用,为RE提供了潜在的治疗策略.
科学领域:
- 胃肠病学 胃肠病学
- 药理学 药理学是指药理学的学科.
- 分子生物学分子生物学
背景情况:
- 逆流性食道炎 (RE) 是一种食道炎症,引起患者严重的痛苦.
- 目前对RE的治疗可能存在局限性,需要新的治疗方法.
研究的目的:
- 在反流性食道炎的老鼠模型中研究阿特拉提利诺利德III (ATLIII) 的治疗疗效.
- 阐明ATL III在治疗RE.治疗中的作用的潜在分子机制.
主要方法:
- 建立了一个反流食道炎小鼠模型,使用手术绑定和酸 perfusion.
- 在28天内通过胃内注射不同剂量的ATL III.
- 通过组织病理学,胃pH值,活性氧物种 (ROS),炎症性细胞因子水平 (TNF-α,IL-8,IL-6,IL-1β) 和关键信号蛋白的西部斑分析 (PI3K/AKT/NF-κB/iNOS) 评估治疗效果.
主要成果:
- 在RE大鼠中,ATL III治疗显著缓解了食道病变,并降低了宏观得分.
- 服用ATL III增加了胃的pH值,降低了ROS和TBARS水平,并降低了炎症性细胞因子的表达.
- 在PI3K/AKT/NF-κB/iNOS通路中的关键蛋白质,包括p-PI3K,p-AKT,iNOS和核NF-κB,被ATLIII调节.
结论:
- 在大鼠模型中,阿特拉提利诺利德III在反流性食道炎中显示出显著的治疗潜力.
- 通过PI3K/AKT/NF-κB/iNOS信号通路,ATL III通过抑制氧化应激和炎症来发挥其保护作用.
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