基酸通过抑制P38MAPK/NF-κB通路来缓解慢性压力诱导的肠损伤
Yuan Zhao1, Chaoran Wang1, Tianyuan Yang1
1Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
慢性压力会损害肠道屏障. 酸 (CGA) 通过抑制p38MAPK和NF-κB通路来保护肠道,恢复肠道屏障功能.
科学领域:
- 胃肠病学 胃肠病学
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 慢性压力会导致肠道屏障受损.
- 线素激活蛋白激酶 (MAPK) 和核因子-卡帕B (NF-κB) 途径与压力诱导的肠道损伤有关.
- 酸 (CGA) 是一种饮食中的多,对肠道有潜在的保护作用.
研究的目的:
- 研究p38MAPK和NF-κB通路在慢性压力诱导的肠壁损伤中的作用.
- 为了确定酸 (CGA) 是否通过调节这些通路来缓解肠道损伤.
主要方法:
- 威斯塔大鼠在21天的时间里遭受了长期的克制压力.
- 干预组接受了SB203582 (p38MAPK抑制剂) 或酸 (CGA).
- 评估了肠道屏障完整性,紧结蛋白表达和酸化MAPK和NF-κB信号分子水平.
主要成果:
- 慢性压力显著增加了p38MAPK的激活,并减少了肠道紧结蛋白 (Occludin,ZO-1,Claudin3).
- 酸 (CGA) 治疗恢复了紧结蛋白的表达,并降低了p38MAPK,p-IκB,p-p65和TNF-α水平.
- SB203582 (p38MAPK 抑制剂) 还改善了紧结蛋白,并减少了p-p65和TNF-α.
结论:
- p38MAPK在慢性压力诱导的肠损伤中发挥着关键作用.
- 酸 (CGA) 通过抑制p38MAPK和NF-κB通路来缓解肠道损伤.
- CGA显示了与压力相关的胃肠道疾病的治疗潜力.
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