通过β-Caryophyllene氧化物刺激血液溶解和红化
Sumiah A Alghareeb1, Mohammad A Alfhili1, Jawaher Alsughayyir1
1Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Saud University, Riyadh 12372, Saudi Arabia.
Life (Basel, Switzerland)
|December 23, 2023
概括
贝塔-卡里奥菲伦氧化物 (CPO) 通过能量耗尽和氧化应激会导致红细胞 (RBC) 损伤,包括血液溶解和红色染色体,通过能量耗尽和氧化应激. 需要进一步的研究,以减轻这些潜在的抗癌治疗开发的不良影响.
科学领域:
- 血液学 血液学 血液学
- 药理学 药理学是指药理学的学科.
- 细胞生物学 细胞生物学
背景情况:
- 抗癌药物可以诱导红血球 (RBC) 中的一种编程细胞死亡形式 - - 红色血球,可能导致贫血.
- 贝塔卡里奥菲伦氧化物 (CPO) 是一种具有抗癌性质的植物性塞斯基特,其对人类红细胞的影响尚未评估.
研究的目的:
- 研究CPO在人体红细胞中的血液溶解和质活动.
- 阐明CPO诱导的红细胞损伤的潜在分子机制.
主要方法:
- 人类红细胞被用不同度的CPO (10-100μM) 治疗.
- 检测包括血液溶解,乳酸脱酶 (LDH),酸氨基转移酶 (AST) 和乙胆酶 (AChE) 活性测量.
- 流细胞计评估了细胞体积,脂 (PS) 外化,细胞内水平和氧化应激.
主要成果:
- CPO诱导了度依赖性血液溶解,LDH和AST泄漏,PS暴露,细胞收缩,细胞内的增加和氧化应激.
- 在CPO治疗后观察到ACHE活性降低.
- 特定的抑制剂 (D4476,稳素,硫胺) 和像ATP和PEG 8000这样的药物改善了CPO诱导的毒性.
结论:
- 通过涉及能量耗尽,流入,氧化应激和关键信号通路 (CK1α,PKC,MLKL) 的机制,CPO刺激红细胞溶血和红细胞溶解.
- 建议在开发CPO作为抗癌剂时谨慎使用,因为它对红细胞有不良影响.
- 与红色体抑制剂,通道阻断剂或抗氧化剂同时使用可能会减轻CPO对红细胞的有害影响.
相关概念视频
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