在臭氧暴露下,牙髓细胞的亡调节和PD-1/PD-L1表达动态 - - 试点方法
Maja Ptasiewicz1, Mirosław Orłowski2, Agnieszka Magryś3
1Department of Oral Medicine, Medical University of Lublin, Lublin, Poland.
Archivum immunologiae et therapiae experimentalis
|September 15, 2024
概括
臭氧暴露会通过改变与细胞死亡和存活相关的基因表达来影响牙纸细胞. 淋巴细胞在免疫检查点分子中表现出极小的变化,这表明它们对氧化应激有弹性.
科学领域:
- 牙纸生物学 牙纸生物学
- 氧化压力研究研究 氧化压力研究
- 免疫学 免疫学 免疫学
背景情况:
- 牙纸细胞对于牙的活力和修复至关重要.
- 臭氧疗法用于牙科,但其细胞效应需要进一步研究.
- 了解细胞对氧化压力的反应是管理牙纸健康的关键.
研究的目的:
- 为了研究臭氧对牙纤维纤维细胞中亲细胞灭亡 (Bax) 和抗细胞灭亡 (Bcl-2) 基因表达的影响.
- 评估免疫检查点分子编程细胞死亡蛋白1 (PD-1),编程死亡连接体1 (PD-L1) 和CD200/CD200R在臭氧暴露后在淋巴细胞上的表面表达.
主要方法:
- 培养了牙纸层细胞,并将它们暴露在臭氧中0,6秒和12秒.
- 实时PCR用于分析Bax和Bcl-2基因表达.
- 使用流式细胞计量测量PD-1,PD-L1和CD200/CD200R在12秒臭氧暴露后的淋巴细胞表达.
主要成果:
- 6秒后的臭氧暴露显著降低了Bcl-2表达和增加了Bax表达.
- 经过12秒的臭氧暴露,Bcl-2表达显著增加,而Bax表达仍然很高.
- 暴露于臭氧12秒的淋巴细胞在PD-1,PD-L1和CD200/CD200R表达中表现出最小的变化.
结论:
- 臭氧暴露会影响牙纸细胞中亡和细胞存活之间的平衡,长时间暴露可能有利于存活.
- 观察到的变化表明牙纸细胞试图抵消长期的氧化应激.
- 在这种情况下,淋巴细胞上的免疫检查点分子PD-1,PD-L1和CD200/CD200R似乎对短期臭氧诱导的氧化应激具有抵抗力.
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