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Updated: Jan 21, 2026

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瘤坏死因子-α对RPMI 2650细胞系的双相作用在体外
Yu V Abalenikhina1, D I Breslavets1, S O Solotnova1
1Ryazan State Medical University, Ryazan, Russia.
Biomeditsinskaia khimiia
|January 20, 2026
概括
瘤亡因子-α (TNFα) 的短期暴露增强了鼻上皮质细胞接触. 然而,长时间的TNFα暴露会触发细胞亡,并增加细胞层的透性,影响炎症性疾病.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 呼吸系统医学 呼吸系统医学
背景情况:
- 瘤亡因子-α (TNFα) 是一种关键的促炎细胞因子,与上呼吸道炎症疾病有关.
- 在各种影响鼻腔通道的炎症状况中观察到TNFα水平升高.
研究的目的:
- 为了研究TNFα对RPMI 2650鼻上皮细胞系的剂量和时间依赖的影响.
- 阐明TNFα诱导的鼻上皮细胞变化背后的分子机制.
主要方法:
- 暴露RPMI 2650细胞在不同时间段 (6-48小时) 的不同度的TNFα (1-100 ng/ml).
- 评估NF-κB激活,细胞亡,细胞活力和细胞间接触蛋白 (E-cadherin,ZO-1) 的水平.
主要成果:
- 短期 (6小时) 的TNFα暴露激活了NF-κB,并增加了E-cadherin和ZO-1水平,而不影响细胞活力.
- 长期 (24-48小时) 的TNFα暴露增加了亲IL-1β,诱导了细胞亡,降低了细胞活力,减少了细胞间接触蛋白.
- 长时间暴露于TNFα导致细胞间接触密度下降,可能增加细胞层的透性.
结论:
- 短期的TNFα暴露可能通过增强鼻上皮的细胞间接触来发挥保护作用.
- 长时间暴露于TNFα会引起有害影响,包括细胞亡和障碍功能受损,有助于疾病的发病.
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