克罗辛对IPEC-J2细胞中过氧化诱导的氧化应激和亡的保护作用
Jing Wang1, Hongbing Song1, Yongjie Huang1
1College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, Fujian, China.
Environmental toxicology
|March 12, 2024
概括
克罗辛通过减少有害分子和防止细胞死亡来保护肠道细胞免受氧化损伤. 这项研究揭示了crocin的存在.
科学领域:
- 细胞生物学 细胞生物学
- 生物化学 生物化学
- 氧化压力研究研究 氧化压力研究
背景情况:
- 克罗辛的抗氧化特性是公认的,但其针对肠道氧化应激的具体机制尚不清楚.
- 肠上皮细胞 (IPEC-J2) 容易受到氧化应激,导致损伤和亡.
- 了解crocin的保护作用对于开发针对肠道损伤的治疗策略至关重要.
研究的目的:
- 研究素对IPEC-J2细胞中过氧化 (H2O2) 诱导的氧化应激的保护作用.
- 阐明克罗辛缓解氧化应激,亡和肠上皮损伤的基础分子机制.
- 分析克罗辛对关键细胞通路的影响,包括Nrf2和线粒体通路.
主要方法:
- 在IPEC-J2细胞中建立了一个H2O2诱导的氧化应激模型.
- 评估了细胞活力,细胞亡,氧化应激标志物 (ROS,MDA,SOD,CAT) 和紧密结合蛋白.
- 使用了甲基 thiazolyl tetrazum 测定,流细胞计,基因/蛋白质表达分析和转录组测序.
主要成果:
- 克罗辛显著降低了活性氧物种 (ROS) 和恶性甲 (MDA) 的水平,同时增加了抗氧化酶 (SOD,CAT).
- 克罗辛通过调节细胞循环因子,线粒体膜潜力和亡途径活性来减弱亡.
- 转录组分析表明,线粒体通路是关键的,而crocin保护了紧密结合蛋白,保持了肠道屏障的完整性.
结论:
- 克罗辛有效地减轻了肠道上皮细胞中的氧化应激和亡.
- 克罗辛通过保持紧密结合蛋白质完整性和氧化还原平衡来保护肠道屏障.
- 这项研究强调了crocin在预防氧化应激引起的肠损伤方面的潜在治疗作用.
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