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素对肠道细胞的毒性导致氧化应激介导的多种细胞死亡途径
Francesco Biscotti1, Massimo Bortolotti1, Federica Falà1
1Department of Medical and Surgical Sciences-DIMEC, Alma Mater Studiorum, University of Bologna, Via San Giacomo 14, 40126 Bologna, Italy.
Toxins
|August 27, 2025
概括
里毒素在摄入后会损害肠道细胞和屏障功能. 细胞死亡途径涉及亡,亡和氧化应激,但可以抑制.
科学领域:
- 毒理学
- 细胞生物学
- 胃肠病学
背景情况:
- 里豆中的强毒素里在口服时构成重大威胁.
- 虽然已知里的全身毒性,但其局部胃肠道效应需要进一步研究.
- 了解瑞对肠道上皮细胞的影响对于评估健康风险至关重要.
研究的目的:
- 对人类肠道上皮细胞系 (HT29和Caco-2) 进行细胞毒性影响的研究.
- 评估瑞对肠上皮屏障的完整性的影响.
- 阐明素诱导的细胞死亡机制,包括亡,亡和氧化应激.
主要方法:
- 用剂量和时间反应测定来评估HT29和Caco-2细胞上的素细胞毒性.
- 通过表皮电阻 (TEER) 测量,评估Caco-2单层表皮屏障的完整性.
- 流细胞测量分析了细胞死亡,并测试了细胞死亡抑制剂和抗氧化剂的作用.
主要成果:
- 在24-72小时后,瑞对HT29和Caco-2细胞具有高细胞毒性,具有纳米EC50值.
- 在24小时内,在0. 1 - 1nM度下,瑞显著降低了Caco-2细胞中的TEER值.
- 通过抑制剂 (Z-VAD,necrostatin-1) 和抗氧化剂 (catalase,BHA,酸盐) 可以预防1nM的细胞死亡.
结论:
- 瑞对人类肠道上皮细胞具有显著的细胞毒性和障碍破坏作用.
- 亡/亡和氧化应激是导致胃肠道里素诱导细胞死亡的关键机制.
- 细胞死亡途径的抑制剂和抗氧化剂显示出缓解辛局部毒性作用的潜力.
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