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拜卡林通过调节IPEC-J2细胞中的AMPK/Nrf2信号通路来减轻H₂O₂引起的氧化应激

Jiahua Liang¹, Ying Zhou¹, Xinyi Cheng¹

¹Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang 330045, China.

International journal of molecular sciences

|June 10, 2023

概括

拜卡林通过增强抗氧化能力和抑制AMPK/Nrf2通路来保护肠道细胞免受氧化应激,从而减少细胞损伤和亡. 这项研究揭示了baicalinalin.

科学领域:

细胞生物学细胞生物学
生物化学生物化学
药理学药理学是指药理学的学科.

背景情况:

由活性氧物种 (ROS) 驱动的氧化应激会损害肠道上皮细胞和屏障功能.
巴伊卡林 (Bai) 是一种草药成分,具有抗氧化和抗炎性质.
过氧化 (H2O2) 是体外模型中氧化应激和细胞损伤的常见诱导因子.

研究的目的:

在IPEC-J2细胞中研究贝卡林对H2O2诱导的肠损伤的保护机制.
阐明AMPK/Nrf2信号通路在贝卡林保护作用中的作用.
评估贝卡林对氧化应激标志物和亡途径的影响.

主要方法:

在IPEC-J2细胞中,用H2O2和不同度的baicalin进行了处理.
评估了细胞活力,细胞亡标志物 (Caspase-3,Caspase-9,FAS,Bax) 和紧密结合蛋白 (ZO-1,Occludin,Claudin1) 的存在.
测量了ROS,MDA水平,抗氧化酶活动 (SOD,CAT,GSH-PX) 和AMPK/Nrf2信号通路组件.
利用短毛RNA (shRNA) 来击败AMPK并评估其作用.

主要成果:

拜卡林治疗减弱了H2O2诱导的IPEC-J2细胞损伤和亡.
贝卡林可以调节紧结蛋白和抗氧化酶活动,同时减少ROS和MDA的产生.
拜卡林通过调节卡斯帕酶和Bcl-2家族蛋白质来抑制亡,并减轻H2O2诱导的Nrf2表达.
贝卡林降低了p-AMPK/AMPK的比率,并且AMPK倒置取消了贝卡林的保护作用.

结论:

巴伊卡林有效地保护肠道上皮细胞免受H2O2诱导的氧化应激和亡.
保护机制包括增强抗氧化能力和改善肠道屏障完整性.
拜卡林通过抑制氧化应激介导的AMPK/Nrf2信号通路来发挥其作用.

关键词:

通过AMPK介导的抗氧化防御.在IPEC-J2 单元中,IPEC-J2 是一个单元.灭症 (apoptosis) 是一种死亡的过程.贝卡林和贝卡林是最重要的.氧化应激是一种氧化应激.

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