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卡塔尔波尔通过激活大鼠肠上皮细胞中的AMPK/mTOR信号通路来改善LPS诱导的炎症反应

Feng Gao¹, Qifu He¹, Shenghui Wu¹

¹Key Laboratory of Animal Biotechnology of the Ministry of Agriculture and Rural Affairs, College of Veterinary Medicine, Northwest A&F University, Yangling, 712100, China.

European journal of pharmacology

|October 27, 2023

概括

卡塔尔波尔是一种天然化合物,通过减少炎症因素和氧化应激,可以防止肠道炎症. 它通过激活肠道细胞中的AMP激活蛋白激酶 (AMPK) 信号通路来实现这一目标.

科学领域:

胃肠病学胃肠病学
细胞生物学细胞生物学
药理学药理学是指药理学的学科.

背景情况:

肠道炎症是一种普遍的临床疾病.
卡塔尔波尔表现出抗炎,抗氧化和抗丧性质,但其在肠道炎症中的确切机制仍然难以捉摸.
了解catalpol的保护机制对于开发新型治疗策略至关重要.

研究的目的:

研究catalpol对肠道上皮细胞中脂聚糖 (LPS) 诱导的炎症的保护作用 (IEC-6).
阐明基底的分子机制,包括参与catalpol作用的信号通路.

主要方法:

用LPS治疗IEC-6细胞以诱导炎症反应.
评估了Catalpol对炎症因子释放 (TNF-α,IL-1β,IL-6),氧化应激标志物 (ROS,MDA,SOD,GSH-PX) 和与亡相关的蛋白质 (Bax,Bcl-2,caspase 3,caspase 9) 的影响.
参与AMP激活蛋白激酶 (AMPK) /哺乳动物目标的拉巴胺素 (mTOR) 信号通路的参与,使用特定的抑制剂,如dorsomorphin.

主要成果:

卡塔波尔剂量依赖地抑制了LPS诱导的炎症因子释放,并抑制了NF-κB信号通路.
卡塔尔波尔通过降低ROS和MDA水平并增强抗氧化酶表达来改善氧化应激.
卡塔尔波尔通过调节关键的亡相关蛋白质的表达来抑制亡,并激活AMPK/mTOR信号通路,这对其抗炎作用至关重要.

结论:

卡塔尔波尔在IEC-6细胞中显示出对LPS诱导的肠炎的显著保护作用.
卡塔波尔的抗炎,抗氧化和抗亡作用是通过AMPK/mTOR信号通路的激活来实现的.
卡塔尔波尔代表了一种有前途的治疗药物,用于控制肠道炎症疾病.

关键词:

在AMPK/mTOR信号通路中.细胞灭亡 (apoptosis) 是一种死亡的过程.加泰罗尼亚,加泰罗尼亚,加泰罗尼亚.肠道炎症是一种肠道炎症.氧化应激是一种氧化应激.

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